DLAT and hepatocellular carcinoma: Upregulation of FDX1 expression enhances lipoylation of DLAT, thereby facilitating the binding of Cu(I) to DLAT, inducing its oligomerization, and subsequently promoting cuproptosis in HCC cells, which could represent the mechanism underlying the improved prognosis observed in patients with HCC characterized by high FDX1 expression (15, 23, 54).