Notably, NLRP3 is associated to myocardial injuries, atherosclerosis and diabetes mellitus (104); Sunitinib, through the induction of iROS and lipid peroxidation, activated MyD88 and NLRP3 increasing inflammation and pro-fibrotic state in cultured cells; notably, treatment with polydatin combined to sunitinib reduced the magnitude of these effects as well as the expression of MyD88 and NLRP3 in a concentration dependent fashion. This evidence concerns the gene NLRP3 and atherosclerosis.