Notably, downregulation of EIF2AK1 signaling following the application of hypomethylating agent (HMA) intervention significantly increased the expression of mitochondrial heme biosynthetic enzymes and iron transport proteins and improved terminal differentiation of SF3B1 mutant MDS-RS erythrocytes, suggesting that the development of EIF2AK1 inhibitors could be a transfusion-dependent way to overcome the transfusion dependence of SF3B1 mutant MDS-RS patients as a viable means to overcome the transfusion dependence of SF3B1 mutant MDS-RS patients (43). This evidence concerns the gene EIF2AK1 and myelodysplastic syndrome.