Momelotinib’s potent and unique (among currently approved and emerging JAK inhibitors) inhibition of hyperactivated ACVR1/ALK2 signaling underlies the suppression of aberrant activation of hepcidin transcription in the liver, increase in circulating iron and hemoglobin, stimulation of erythropoiesis, and its consequent marked benefit on iron-restricted anemia, including reversal of RBC transfusion-dependence in MF patients [67]. The gene discussed is ACVR1; the disease is anemia (phenotype).