Our in silico results predicted outcomes for the hypothesized mechanisms were able to explain conflicting RAS peptide alterations in ANGI and ANGII from two previous experimental studies of patients with different COVID-19 severity [1,6] by considering the variations in homeostasis RAS peptides due to premorbidity and feedback of ANGII⋅AT1R to renin. The gene discussed is AGT; the disease is COVID-19.