In keeping with the post‐absorptive leg protein breakdown responses and lack of difference in muscle mass between statin myalgia and control volunteers, the post‐prandial increase in muscle protein synthesis was not blunted in statin myalgia, and contrasts what might have been expected based on the disruption of PI3k/Akt signalling in rodent statin myopathy (Mallinson et al. Here, AKT1 is linked to myopathy.