Altogether, these findings highlight a mechanism by which cancer cachexia-associated IL-6 family cytokines induce ATGL/CGI-58-dependent lipolysis and adipose wasting through JAK/STAT3 signaling and subsequent de novo transcription/translation, diverging significantly from the traditional sympathetic β-adrenergic induction of adipocyte lipolysis. This evidence concerns the gene STAT3 and cancer.