Diabetes significantly reduced plasmaIGF-1 levels, whereas B12 restored them through DNA methylation of S-adenosylmethionine levels, DNMT-1/3a/3b mRNA, and suppressing cytokine signaling (SOCS)-1/3 promoters normalization to activate hepatic IGF-1 production, and reductions in cardiac IGF-1 mRNA and phosphorylated IGF-1 receptors were also restored, predicting B12 as a promising potential treatment for DCM (113). This evidence concerns the gene IGF1 and familial dilated cardiomyopathy.