First, the presence of exacerbated dilated cardiomyopathy in females compared to males and a similar electrical remodelling support the notion that the higher mortality in female AT1R mice is not associated with alteration in ionic currents but rather from a mechanical dysfunction, poor Ca2+ handling and more severe ventricular hypertrophy and dilation, findings that would be compatible with a PEA. This evidence concerns the gene AGTR1 and cardiac hypertrophy.