Since NF-κB signaling, defective insulin signaling, JNK signaling, and alterations in autophagy have been implicated in the pathogenesis of diabetic cardiomyopathy [19, 70–72], we next determined if MuRF2−/− hearts had alterations in these processes that may explain their more severe phenotype. This evidence concerns the gene INS and diabetic cardiomyopathy.