To our surprise, MuRF3−/− hearts hypertrophied to the same degree as wildtype controls over time (Fig. 1d, Fig. 2e, Table 1), illustrating either MuRF3 minimal contribution to regulating SRF during the development of diabetic cardiomyopathy or potentially its redundant regulation of SRF with other MuRF family members. Here, TRIM54 is linked to diabetic cardiomyopathy.