A growing body of research has linked RBPs—such as human antigen R (HuR), sequestosome 1 (p62), polypyrimidine tract-binding protein 1 (PTBP1), and heterogeneous nuclear ribonucleoproteins (hnRNPs)—to lipogenesis and inflammation, both of which contribute to NAFLD through mechanisms involving transcriptional regulation, alternative splicing, RNA stability, polyadenylation, and subcellular localization. Here, ELAVL1 is linked to metabolic dysfunction-associated steatotic liver disease.