Nevertheless, the observation of tumor-induced IL-6 reprogramming hepatic ketogenesis, when taken together with the recent report of lung cancer rewiring hepatic circadian homeostasis involving insulin, glucose, and lipid metabolism (Masri et al., 2016), suggests that the liver may be a specific target of tumor-induced effects on the host, presumably for the benefit of the tumor and the detriment of the host. This evidence concerns the gene INS and lung cancer.