IL17A and metabolic dysfunction-associated steatotic liver disease: In hyperlipidaemia and NAFLD patients systemic overexpression of genes involved in SARS-CoV-2 entry and cleavage (such as FURIN, angiotensin I converting enzyme 2, and transmembrane serine protease 2), (35–37) pro-inflammatory M1 phenotype polarization of macrophages mediated by interferon, circulating levels of pro-inflammatory cytokines elevated, increased neutrophil-to-lymphocyte ratio with activation of the pro- interleukin-17 axis, and enhanced production of pro-coagulant molecules, (38–43) these pathways increase susceptibility of severe COVID-19 in NAFLD patients.