It is therefore tempting to assume that the enhanced vulnerability of severe, decompensated CHF to COVID‐19 manifestations may stem from an inadequate ACE2 compensatory response along with a depletion of the tissue‐protective Ang 1‐7, leading to an unrestricted stimulation of the harmful arm of RAAS, that is, ACE/Ang II/AT‐1. This evidence concerns the gene ACE and COVID-19.