APOB and COVID-19: Notably, HEP4 hepatocytes also exhibit low HNF4A, APOB, and high SCARB1, STAT3, and HIF1A, a phenotype identified using bulk proteomics on severe COVID-19 patient livers, and hypothesized to be driven by the combination of hypoxia and activation of STAT3, leading to a reduction of the differentiated hepatocyte pathways orchestrated by downregulation of HNF4A [32].