In this sense, it is noteworthy that the mRNA expression of this potentially metabolically beneficial endogenous antagonist of ghrelin action is stimulated in vitro by, and correlates in vivo with, non-CB1-mediated (and hence non-metabolically “noxious”) eCBome signaling, i.e., respectively: (1) activation of PPARγ, which is known to be an intermediate in anti-diabetic and anti-glucose intolerance drugs, and (2) expression of PPARα and the levels of one of its endogenous agonists, i.e., 2-PG, with potential anorectic and anti-dyslipidemic actions. The gene discussed is GHRL; the disease is Glucose intolerance.