Whereas in VEXAS syndrome, UBA1 mutations alone are thought to drive both the inflammatory and MDS phenotypes, in UBA1‐wildtype patients with MDS/CMML, early somatic mutations in TET2/IDH1 (and/or SRSF2) are thought to contribute to the MDS/CMML and SIAD components [7, 8]. The gene discussed is TET2; the disease is chronic myelomonocytic leukemia.