External use of sulfonylureas (such as Glibenclamide) can inhibit the activation of NLRP3, up-regulate IL-10, IGF-1 and TGF-β, down-regulate IL-1β, IL-18, and TNF-α, and as a result down-regulate the pro-inflammatory M1 phenotype, up-regulate the pro-healing M2 phenotype and promote wound healing in DM mice (Mirza et al., 2014). This evidence concerns the gene IL1B and diabetes mellitus.