We also aimed to further explore the putative pathological interaction between the lack of endogenous CORT or SST and MGT in the context of an extreme metabolic condition, such as diet-induced obesity, because the SST/CORT system has been shown to play a crucial role in the regulation of the adaptive mechanism triggered in response to obesity [24, 57], which, in turn, has been directly associated with the development and progression of MG tumorigenic processes in mouse models [58, 59] and in humans [25, 26]. This evidence concerns the gene CORT and obesity disorder.