Another hypothesis for the cardiac involvement in COVID-19 implicates the systemic release of pro-inflammatory cytokines (e.g., IL-1, IL-6, TNF-α, IFN-γ, and MIP) and the subsequent “cytokine storm” as the main culprit with subsequent increased vascular wall permeability and myocardial edema [11]. This evidence concerns the gene MIP and COVID-19.