Several recent studies have linked TET2 to inflammatory responses and connected loss of TET2 to inflammation-driven clonal hematopoiesis, pre-leukemia, and MDS.14, 15, 16, 17, 18, 19 The effects of TET2 on repressing inflammation have been assigned to its methylcytosine dioxygenase activity but also to its ability to recruit histone deacetylase (HDAC)-mediated repressor activity to pro-inflammatory genes.17 This evidence concerns the gene HDAC9 and leukemia.