Endothelial dysfunction reduces muscle protein synthesis by compromising the delivery of nutrients into skeletal muscles and hampering their utility,8, 9, 10, 22 whereas ischaemia and reperfusion injury resulting from lower extremity atherosclerosis accelerate muscle protein degradation through mitochondria dysfunction, enhancement of reactive oxygen species and oxidative stress and activation of inflammatory and the transforming growth factor‐beta (TGF‐β) pathway.11, 23. The gene discussed is TGFB1; the disease is atherosclerosis.