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Apple’s price hikes are a warning to IT
IT purchasing is being hit by a double-whammy: Enterprises want to ensure their hardware is good enough to support AI, even as memory shortages caused by AI deployments are driving steep price increases for Macs, iPhones, iPads, tablets, Android devices and Windows PCs.
The root cause is widely known. JP Morgan estimates DRAM prices have risen more than 400% since the beginning of 2024 as data center construction and hyperscaler demand consumed a gargantuan chunk of global memory production capacity.
More pain is coming“It is not a secret that the industry will stay in shortage for multiple years,” warned analyst Jay Kwon. IDC analysis expects DRAM manufacturing capacity to fall short of demand, while SK Hynix believes demand will exceed supply well into the next decade. AI data centers are absorbing around 70% of output.
This tough provisioning juggling act plays out as economic insecurity continues and the supply of key materials beyond memory also remains constrained. It makes for a perfect storm of shrinking purchasing budgets, rapid price increases, and competitive pressure to accelerate ongoing patterns of digital transformation.
To some extent, business leasing schemes will probably become more popular, while IaaS and SaaS vendors will widen their offerings to also include the kind of AI services businesses need. But the scale of the problem is pretty clear:
- Apple recently imposed roughly 20% price increases across all its hardware, with the exception (for now) of iPhones. The latter are expected to see their own price increases in the coming weeks as the company grapples with the reality that memory price inflation has made its products 38% more expensive to build.
- Huawei Executive Director and Consumer Business Group Chair Richard Yu warned that rising memory costs will force his company to hike prices to “relieve the ever-increasing cost pressure.”
- Despite making memory itself, Samsung has also implemented rolling price increases across multiple smartphone and tablet ranges, up to $120 more in some cases.
- Google is expected to raise prices across the Pixel line, probably when it introduces its new devices on Aug. 12.
- Motorola slapped price hikes of up to 50% on its Moto G smartphones in April.
- Xiaomi raised its own prices by up to 13% in China.
- Dell, Lenovo, HP, and Acer have all increased prices — even as Microsoft hits its struggling OEMs with its own 10% price hike on Windows 11 licenses.
These price increases are not isolated; they reflect the global memory price challenge. Gartner expects memory prices will increase roughly 130% by the end of the year, while TrendForce’s recent survey sees further DRAM price increases ahead.
No one will be sparedThis is a global challenge affecting businesses and consumers everywhere in real time. What’s important about these price hikes is their unpredictability; in most cases, business leaders will not have known the increases were coming, which means existing, pre-determined purchasing budgets do not reflect this new reality.
“The IT landscape faces a seismic shift, and its epicenter is memory,” according to Insight. “The market dynamics have fundamentally changed.” In other words, this challenge is long-term, structural, and here to stay.
As a result, every device that contains memory or a processor will get more expensive; this is already particularly visible in networking equipment, the cost of which climbed up to seven-fold in some cases this year. Games consoles, smart TVs and streaming boxes — including Apple TV — have not been spared.
IT purchasers are looking at these trends and wondering what to do. When it comes to PCs, price unpredictability means that lower cost isn’t necessarily an advantage. It makes more sense to spend a little more today to end up with a system that can continue working for your business for five years or more. Purchasers want longer hardware life cycles and are more willing than they once were to look at refurbished devices, which is driving growth in reconditioned markets.
(Apple sees this, which is why it recently raised trade-in prices for its kit as it seeks to recondition and resell its own products where possible.)
Reliability, resale value, and recycling and energy costs need to be considered, concerns that are in part driving businesses toward Macs. Regular readers will recognize the numbers often add up. Forrester’s Total Economic Impact research says lower support costs mean Macs save hundreds of dollars per seat in comparison to PCs over just three years, while Cisco has reported significant cost savings.
So, what should IT purchasers do?Waiting for prices to stabilize isn’t a strategy. All the analyses show there will be no change for some time. Seeking some resilience, purchasers are seeking multi-year leasing agreements and bulk purchase deals even while vendors become more resistant to them.
Three-year replacement cycles are being extended, prompting purchasers to make better buying decisions in the first place, and canny buyers should already be auditing what roles need what kind of machine. Does every computer need to be AI-ready? Probably not, so it’s important not to over-spec the whole fleet.
Many purchasers will likely be investing more in Macs as they seek to diversify vendor exposure, while total cost of ownership over time is becoming a far more significant concern than before. It really matters that Macs are cheaper to run over time than PCs, particularly when costs have become so unpredictable. The same logic applies to tablets and smartphones, too.
None of these steps take the problem away. But sensible decision making now could help manage what is likely to be a highly uncertain period in IT purchasing, reiterating the need for resilience, so anticipated price shocks don’t blow your budgets apart.
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Million-Person Study Finds a Rare Gene Variant That Slashes the Risk of Diabetes and Heart Disease
The discovery could lead to treatments and demonstrates the power of efforts to unearth rare, beneficial genes in large populations.
“Burn fat, build muscle.” It’s a familiar workout slogan, but the benefits go far beyond aesthetics. Having less belly fat and more muscle guards against heart attacks, Type 2 diabetes, and a host of other metabolic diseases.
Some people may have a genetic edge.
A massive study of over one million people across three continents discovered a rare mutation in a gene called FNIP1 is linked to a healthier metabolic profile. The gene helps cells sense nutrients and generate energy. All of us have FNIP1, but about one in 7,000 people inherit a protective version. On average, they had a 60 percent lower risk of heart disease and metabolic disorders.
Silencing FNIP1 in human liver cells switched on a genetic program that breaks down fats. In mice fed a tasty but high-fat diet, disabling the gene curbed weight gain, prevented fatty liver disease, improved insulin sensitivity, and kept their blood sugar levels steady.
The findings are great news for everyone else. Rather than relying on a naturally occurring mutation, future gene editing therapies could potentially recreate its protective effects in people against a host of cardiometabolic diseases, a leading cause of death worldwide.
Everyone has a unique metabolic profile shaped by both genes and environment. By analyzing diverse populations, the study fished out a protective variant that spans ancestries and lifestyles. The broad reach suggests targeting FNIP1 could benefit people around the world.
The study illustrates the power of efforts to find rare, beneficial genes across large populations, wrote the authors at Regeneron Pharmaceuticals, a New York biotechnology company.
Mutant ProtectorSmall changes in DNA can have large consequences. Some genetic variants raise the risk for health issues. The APOE4 variant, for example, increases the chances of developing Alzheimer’s disease. Others, however, are a gold mine for new treatments.
A notable example is CCR5. People who inherit a rare mutation in both copies of thegene are naturally resistant to HIV. The mutation prevents the virus from tunneling into immune cells and replicating. The discovery has led to multiple success stories in which bone marrow transplants from donors carrying the mutation kept HIV at bay, without the need for lifelong antiviral drugs.
Protective mutations could also lower the risk of heart disease. Rare variants of PCSK9, a gene involved in cholesterol metabolism, disable the gene and slash dangerously high levels of LDL, or “bad” cholesterol that clogs arteries. The discovery has already spurred a handful of therapies that block the gene or its protein with early successes.
“Identifying genetic variants associated with protection from disease is a powerful strategy,” wrote the authors. “However, protective genetic variants are often extremely rare, so finding them requires sequencing the genomes of large populations.”
Go BigTo better understand cardiometabolic diseases, the team sequenced the genomes of over a million people from 11 studies across the Americas, Europe, and Asia, including people with African ancestry. They also linked genetic data with participants’ health records.
The researchers searched for gene variants that influence a blood biomarker for cardiometabolic disease. Called TG:HDL, the biomarker is the ratio between two types of fats. The first, triglycerides, is packaged into tiny “bubbles” that circulate the bloodstream. High levels are linked to heart attacks, strokes, and other metabolic problems. In contrast, high-density lipoprotein, often called “good” cholesterol, ferries excess fat away from tissues and blood vessel walls to the liver, where it can be cleared.
Across the populations in the study, a lower TG:HDL ratio—that is less TG, more HDL, or both—tracked with better metabolic health. People with lower ratios had reduced insulin levels, lower blood pressure, and less fat buildup in the liver and muscles. The biomarker also predicted diabetes risk, heart problems, and liver scarring, making it a powerful snapshot of overall metabolic health.
The team then scanned the genome for rare gene variants linked to TG:HDL. Roughly 60 genes popped up, all involved in energy storage and active in the liver and fat tissues.
But one gene stood out: FNIP1. Rare variants essentially disable the gene by disrupting its protein-making instructions. People with one copy of these variants had lower liver fat and blood sugar and roughly 60 percent lower risk of cardiometabolic disease.
The finding “was remarkable and thought-provoking, and immediately motivated us to dig deeper into the biology of this discovery,” wrote the team. But a key question remained: Were the variants actually protecting people, or were they simply correlated with better health?
To find out, the team silenced the gene in human liver cells using a method called siRNA. Rather than snipping the gene, siRNA blocks cells from producing targeted proteins. Without functional FNIP1, liver cells ramped up genes involved in breaking down fats.
The researchers then turned to mice. Using CRISPR-Cas9, they got rid of FNIP1 and related signaling pathways specifically in mice fed a high-fat, high-sugar diet. The intervention rapidly activated mitochondria—the cell’s energy factories—and lysosomes, the acid-filled recycling centers that break down waste. Despite gorging on the unhealthy diet, mice lacking functional FNIP1 had less body and liver fat, more muscle mass, and better sensitivity to insulin.
That’s not to say FNIP1 is a “villain” gene. Normally, it acts as a metabolic brake, helping the body conserve precious energy when food is scarce. But many of us now face the opposite problem, an abundance of calories and not enough physical activity. Releasing that brake, through medication or gene editing, could rev up the body’s natural fat-burning machinery.
Turning the finding into a therapy won’t be simple. The protective effects were found in people who carried the mutation from birth. A short-term drug or gene therapy delivered later in life might not reproduce the same effects.
Safety is another major concern. Paradoxically, people who have mutations in both copies of FNIP1 develop heart disease and immune deficiency. And mice without functional FNIP1 throughout the body are more prone to liver damage and cancer. Targeting treatments specifically to the liver—for example, using lipid nanoparticles—could limit side effects, but any potential therapy will need to be thoroughly tested for safety.
The team is searching for drug candidates that inhibit FNIP1. But for now, they’ve shown the power of large-scale genetic screens across diverse populations to find rare protective variants—and potential paths towards treating diseases that affect millions of people.
“Identifying FNIP1, a previously poorly characterized gene involved in lipid metabolism, is highly novel and promising for future drug development for metabolic health,” Satoshi Koyama at the Broad Institute, who was not involved in the study, said in a research briefing. “I sincerely hope that this discovery will one day benefit patients with metabolic disorders.”
The post Million-Person Study Finds a Rare Gene Variant That Slashes the Risk of Diabetes and Heart Disease appeared first on SingularityHub.
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