In patients with T2DM, a hyperglycemicenvironment stimulates activated monocyte-macrophagesto synthesize IL-1β and IL-18 in largequantities, which in turn activates renal tubularepithelial cell nuclear transcription factor (NF-KB),exacerbates inflammatory responses, and enhancesthe promotional effect of transforming growth factor-βon renal fibrosis [22].The precursor forms of IL-1βand IL-18 are inactive and need to be cleaved by caspase-1 to exert a pro-inflammatory response, andcaspase-1 is the end product of cleavage of pro-caspase-1 by NLRP3. This evidence concerns the gene NFKB1 and type 2 diabetes mellitus.