IL4 and metabolic dysfunction-associated steatohepatitis: In order to assess the ability of LIVRQNac to directly modulate drivers of NASH pathogenesis, we initially leveraged three primary human cell model systems that capture several NASH-relevant phenotypes: metabolic dysregulation in a primary human hepatocyte (PHH) model of lipotoxicity31, inflammation in a lipopolysaccharide (LPS)/interleukin-4 (IL-4)-stimulated primary human macrophage (PHM) model32, and fibrosis in a transforming growth factor-beta 1 (TGF-β1)-stimulated primary human hepatic stellate cell (HSC) model33.