The authors speculated if the discovery that mutations in TET2 [150, 162, 163, 166], DNMT3A [161], and IDH1/2 [167] elicit an increased self-renewal might actually negatively influence the ability of IFN-alpha2 to reduce or eliminate mutant MPN disease initiating cells, which harbor these mutations and accordingly conferring acquired resistance to IFN-alpha2 [36]. The gene discussed is TET2; the disease is myeloproliferative neoplasm.