Furthermore, SGLT2i improved hepatic steatosis by decreasing NLRP3 (nucleotide-binding domain, leucine-rich repeat-containing family, pyrin domain containing 3) inflammasome activation, significantly inhibiting the production of interleukin (IL)-1, IL-6 or tumor necrosis factor-alpha (TNF-alpha), and improving hepatic steatosis [55,56]. This evidence concerns the gene NLRP3 and fatty liver disease.