TLR4, which upregulates IL-1, has been shown to control muscle wasting during Lewis lung carcinoma-induced cachexia82; and mice deficient in MyD88, the signaling adaptor downstream of IL-1R and most TLRs, are protected from fat and muscle loss, fatigue, and mortality in a pancreatic cancer model of cachexia83. This evidence concerns the gene IL1B and pancreatic neoplasm.