Additionally, prior studies did not investigate the direct effect of MC38 tumor cells on muscle atrophy in vitro, whereas we showed marked muscle atrophy in C2C12 myotubes exposed to MC38 cells, consistent with the increased phosphorylation of STAT3, a key mediator of muscle wasting in cancer cachexia [9,12,13,17,20]. This evidence concerns the gene STAT3 and cancer.