It is possible that in the initial phase of NAFLD, NLRP3 and NLRP6 act by inducing IL-18 secretion and thus its beneficial effects on the microbiota to protect and slow the progression of the disease, whereas with prolonged persistence of NAFLD-inducing triggers, the adverse, pro-inflammatory effect of IL-1β predominates and NLRP3 then contributes to the progression of liver degeneration, inflammation, and fibrosis. This evidence concerns the gene NLRP3 and metabolic dysfunction-associated steatotic liver disease.