The mechanism underlying this elevated risk might include excess fatty acid synthesis and hepatic steatosis caused by ritonavir [22]; protection of apolipoprotein B, an LDL component, from degradation by the proteasome [23]; and interactions with cellular retinoic acid binding protein 1 or lipoprotein receptor-related protein by PIs, leading to alterations in the lipid profile [15, 24]. Here, APOB is linked to Hepatic steatosis.