Specific RNAi-mediated knockdown of ImpL2 in the adult ykiact gut tumors or in the RasV12 scrib−/− adult tumor models restored insulin signaling in peripheral tissues and ameliorated the muscle phenotypes without affecting tumor growth (Figueroa-Clarevega and Bilder, 2015; Kwon et al., 2015), demonstrating that a tumor-derived factor can disrupt insulin signaling and drive organ wasting (Wagner and Petruzzelli, 2015). The gene discussed is INS; the disease is neoplasm.