We found that COVID-19 patients have a significant age-associated increase of autoantibody levels against 16 targets (e.g., amyloid β peptide, β catenin, cardiolipin, claudin, enteric nerve, fibulin, insulin receptor a, and platelet glycoprotein), which provides new avenues for mechanistic validation of these targets within the clinical context of their pathophysiology. The gene discussed is INSR; the disease is COVID-19.