Future studies should (i) clearly define tissue source and assay modality, (ii) distinguish membrane-bound from soluble ACE2, (iii) determine whether observed changes are compensatory or pathogenic, and (iv) integrate tissue-level, genetic, and functional data to better define how RAAS dysregulation links diabetes to both SARS-CoV-2 susceptibility and DCM. This evidence concerns the gene ACE2 and familial dilated cardiomyopathy.