Pathogenesis of COVID-19 cardiomyopathy is intimately related to inflammatory cytokines, referring here to diastolic dysfunction and increased myocardial stiffness mediated by interleukin-6 (IL-6), negative inotropic effects exerted by interleukin-1β (IL-1β), or myocardial fibrosis induced by IL-1β and tumor necrosis factor alfa (TNF-α). This evidence concerns the gene IL1B and COVID-19.