This hypothesis is further supported by the fact that several of the elevated cytokines in the circulation of patients with severe COVID-19 [37, 38], such as CCL2 and TNF-α, have a crucial role in the development and progression of NAFLD by recruiting inflammatory cells in the liver or by regulating hepatocyte apoptosis [39]. The gene discussed is CCL2; the disease is metabolic dysfunction-associated steatotic liver disease.