From some recent reports that examined the role of PKCs and MAPKs in the development and/or progression of diabetic nephropathy, PKC was reported to directly activate ERK and JNK pathways [54,55], leading to overexpression of TGF-β that promotes cardiomyocyte remodelling, especially hypertrophy, which only worsens over time [56,57]. This evidence concerns the gene PRRT2 and diabetic kidney disease.