Thus, a model for the triggering mechanism of ARDS and associated cardio-respiratory instability in the hyper acute cases of COVID-19 would be direct involvement of the virus causing decreased ACE2 availability and subsequent reduction on BK degradation via spike protein-dependent interactions, leading to increased downstream BK signaling in the endothelial cells via BKRB2, alveolar capillary leak, and infiltration of activated immune cells (43). The gene discussed is ACE2; the disease is acute respiratory distress syndrome.