It is, therefore, of growing interest to find strategies to selectively modulate the function and polarity of KCs, both to potentially control their distribution and behavior, and to be able to modulate their phenotype depending on the pathophysiological context, to modify their cross-talk with other cells in the liver niche, in particular hepatocytes in the context of atherosclerosis and MASLD. The gene discussed is TBCE; the disease is metabolic dysfunction-associated steatotic liver disease.