TBCE and metabolic dysfunction-associated steatotic liver disease: Future research should aim to fill some interesting gaps related to KC biology, such as (i) unraveling the mechanism underlying the loss of lipid uptake capacity of EmKCs under conditions of lipid overload and how this might affect hypercholesterolemia dependent generation of dysfunctional KCs; (ii) understand the paracrine signals within the hepatic niche that may activate stellate cells, thus leading to the increase in fibrosis and exacerbate MASLD progression.