The lack of effective medications for treating the metabolic syndrome in general, on one hand, and the key physiological and pathological roles that the eCB/CB1R system plays, on the other hand, as well as evidence on the specific deletions of CB1R in the liver, adipose tissue, kidney, pancreas, and skeletal muscle, have underscored its importance in modulating peripheral metabolic function [28,29,39,40,[55], [56], [57]]. The gene discussed is CNR1; the disease is metabolic syndrome.