Continuously increased muscular TRIM62 expression throughout the disease course in ICUAW patients and in all mouse models was in clear contrast to the time course of the commonly used atrophy markers Atrogin1 and MuRF1, which are rapidly, but only transiently, increased in muscles of critically ill patients [8] and murine muscle atrophy models [12]. This evidence concerns the gene TRIM62 and muscle atrophy.