Our study suggests that ICAM1, MMP9, TLR2, and SOCS3 are a promising intervention target: SARS-CoV-2 infection aggravates the endothelin induction in multiple organs of COVID-19 patients via viral involvement in the host inflammatory and immune response, and the presence of elements within endothelial cells and the gathering of inflammatory cells (Varga et al., 2020). The gene discussed is TLR2; the disease is COVID-19.