Hence, it is possible that the interaction between Nod2 and the Nlrp1b2 inflammasome (C57BL/6) is not as efficient, as the interaction of Nod2 with the Nlrp1b1 inflammasome (Balb/c), in promoting caspase-1 activation and IL-1β production in the colon, to prevent dysbiosis in response to a HFD, thus facilitating glucose metabolism alterations, dyslipidemia and ultimately T2D. The gene discussed is CASP1; the disease is metabolic syndrome.