Given that in the Nlrp1 deficient mice the Nlrp1a and Nlrp1c genes were also eliminated10 and that these genes are identical among mouse strains, our data together with that of Murphy et al. 10, suggest that i) the Nlrp1b gene is involved in attenuating the inflammatory response in the adipose tissue and promoting lipolysis in response to a caloric excess and ii) that the gene products of different alleles of the Nlrp1b gene have different efficacies to promote IL-18 production and therefore, to protect from dyslipidemia and T2D in obese animals. The gene discussed is IL18; the disease is type 2 diabetes mellitus.