Yin et al. (2019) show that miR-30c protects cardiac metabolism and function in diabetes through PPARα modulation and its downstream effector, the co-activator Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α). The miR-208a, whose overexpression induced spontaneous cardiac hypertrophy (Callis et al., 2009), is another miR playing a role in DCM. Recently, Lum-Naihe et al. (2017) highlighted higher miR-208a expression in female diabetic hearts than in male counterparts. Here, PPARGC1A is linked to cardiac hypertrophy.