Inhibition of hepcidin by variant ERFE may be responsible for the increased iron load in SF3B1 mutant MDS patients, and the use of hepcidin agonists or targeting ERFE overexpression may provide a potential therapeutic strategy for preventing iron overload and improving erythropoiesis in SF3B1 mutant MDS patients (49). The gene discussed is SF3B1; the disease is myelodysplastic syndrome.