2009, 2012). In keeping with this, statin myalgia in the present study was associated with increased expression of genes involved in muscle proteolysis (MuRF1, MMP2), apoptosis (Caspase 8/9, BCL2, RhoB, MMP2, myostatin) and autophagy (TFAM, BNIP3) (Fig. 7). However, these differences in mRNA abundance were modest and did not translate into increased leg protein breakdown, even under post‐absorptive state conditions where the rate of leg protein breakdown would predominate over synthesis (Fig. 5B), or reduced leg lean mass (Fig. 2). The gene discussed is TRIM63; the disease is Myalgia.