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. The gene discussed is NFKB1; the disease is diabetic cardiomyopathy.