The activation of these inflammatory signals induces anorexia and gastrocnemius catabolism.73 Dilp8/INSL3 derived from tumor tissue activates the Lgr3 receptor in the hypothalamus, which increases the expression of anorexigenic nucleobinding 1 and decreases the expression of the orexigenic neuropeptides short neuropeptide F (sNPF) and NPF, triggering cachexia-associated anorexia.74 In addition to peripheral tissue-derived inflammatory molecules, the neuroimmune axis has recently been implicated in cachexia in mouse models and human specimens. The gene discussed is INSL3; the disease is Cachexia.