We’ve reviewed the available evidence on myostatin gene inactivation in humans, and what we’ve found so far is that 81 assertions support the idea that turning off this gene leads to an increase in skeletal muscle mass, with no assertions contradicting it [1]. Myostatin is a protein that normally limits how much muscle tissue can grow; when its activity is reduced, muscle fibers may grow larger or more numerous. These assertions are based on observations in rare human cases where natural mutations or medical interventions reduced myostatin function, resulting in noticeably higher muscle mass compared to typical individuals. While the number of assertions is high, it’s important to note that these are not controlled studies with large groups of participants. Most of the evidence comes from isolated cases — such as individuals born with genetic mutations affecting myostatin — rather than clinical trials or population-wide data. We don’t have information on long-term effects, safety, or how consistent this outcome is across different people. The evidence we’ve reviewed leans toward the idea that reducing myostatin activity in humans is linked to greater muscle mass, but we cannot say how reliably this can be triggered, or whether it applies to everyone. There’s also no data yet on whether this change affects strength, metabolism, or overall health in the long term. For now, this suggests that myostatin plays a role in limiting muscle growth in humans, and interfering with it may lead to more muscle — but we’re still far from understanding how to do this safely or effectively outside of rare genetic conditions.