We could not exclude the compensatory effect from S6K2 contributing to the myopathy in S6K1‐TSC1mKO mice, yet a similar phenomenon has been observed in AKT‐stimulated muscle hypertrophy, where S6K1 inactivation did not limit cellular growth but exacerbated the accumulation of p62 aggregates and decreased force production in muscle with AKT hyperactivation (TgAkt‐S6K1KO mice).39 This evidence concerns the gene AKT1 and myopathy.