We propose that in cancer cachexia, increased FoxO3 occupancy at pro-atrophic genes MuRF1, MAFbx/Atrogin-1, and GABARAPL1 is promoted by AMPK-mediated FoxO3 phosphorylation, which is ultimately induced by increased systemic IL6 levels and AMPK activation in skeletal muscle (Fig. 10). This evidence concerns the gene FBXO32 and cancer.