Recently, we showed that CB activity is increased in prediabetes and type 2 diabetes animal models [13,18,19,20] and patients [21] (Figure 1a) and that the abolishment of CB activity in animals, via chronic resection of the CSN or CB ablation, prevents and reverses dysmetabolism in rodent models of metabolic disease [13,15,16] (Figure 1b) by positively impacting glucose uptake and insulin signaling in the liver and in the visceral adipose tissue [15]. The gene discussed is INS; the disease is Other metabolic disease.