An interesting study by Daniel et al. showed that Pb exposure may favor NAFLD by lowering the levels of sorcin, a protein that confiscates ChREBP (carbohydrate-responsive element binding protein) within the cytoplasm, thus enhancing the nuclear shuttling and transactivation of ChREBP, that results in increased hepatic DNL [145] (Figure 3). The gene discussed is MLXIPL; the disease is metabolic dysfunction-associated steatotic liver disease.