CAMK2G and cardiomyopathy: Ikeda et al. showed that FIR therapy can increase endothelial nitric oxide synthase (eNOS) mRNA expression, eNOS protein production, and nitric oxide (NO) levels in cardiomyopathy and heart failure [44], which may be related to the pathway of increasing Ca2+/calmodulin-dependent protein kinase (CaMKII)-mediated eNOS phosphorylation [45].