Although Prdm16Q187X/WT × Prdm16WT/WT offspring showed a Mendelian distribution, there was a slightly lower-than expected proportion of female Prdm16Q187X/WT mice born (Figure 3K).60 These findings once again highlight sexual dimorphism in PRDM16-related cardiomyopathy in preclinical animal models. This evidence concerns the gene PRDM16 and cardiomyopathy.