The potential explanations may have three points: (1) anti-TNFα treatment downregulated IFN-γ which would induced the expression of ACE2 through downregulating IFN-γ (32); (2) anti-TNFα treatment also downregulated other proinflammatory cytokines in “TNF dependent cytokine cascade,” such as IL-1, IL-6 and IFN-γ which also play important roles in cytokine storm syndrome in COVID-19 (32); (3) anti-TNFα could induce a reduction in leucocyte trafficking due to reduction of adhesion molecules, vascular endothelial growth factor and chemokines in both IBD and COVID-19 (33, 34). The gene discussed is ACE2; the disease is COVID-19.