It is established that the cardiomyocyte pyroptosis plays an important role in the development of DCM.1 Silencing NLRP3 was reported to suppress pyroptosis in H9c2 cardiomyocytes under high-glucose concentration and improve cardiac inflammation, pyroptosis, and fibrosis in Type 2 diabetes mellitus (T2DM) rats.12 In addition, caspase-1-induced pyroptosis in DCM is related to ncRNAs including microRNA-30 (miR-30).13 and long ncRNA (lncRNA) Kcnq1ot1c.14 Therefore, we believe that inhibiting of cell pyroptosis may offer a new therapeutic strategy for diabetic cardiomyopathy.10 This evidence concerns the gene CASP1 and familial dilated cardiomyopathy.