FBXO32 and Cachexia: In cachexia and chronic kidney disease models, both of which exhibit muscle mass loss, STAT3 initiated muscle wasting by stimulating CCAAT/enhancer binding protein (C/EBPδ) expression and activity, which in turn increased myostatin, MAFbx/Atrogin-1, and MuRF-1 expression in myofibers (Zhang et al., 2013).