These findings provide a new therapeutic strategy for selective targeting of cells bearing TET2 mutations.252 5-azacytidine, a DNA demethylating agent, shows higher cytotoxicity in TET2-silenced cells, probably due to the hypermethylation pattern caused by the loss of TET2.256 In addition, C35, a selective TETs inhibitor, promotes somatic cell reprogramming.250 As a robust TET2 activator, clinical trials are investigating the effects of Vitamin C on hematologic malignancy patients with TET2 mutations (NCT03397173; NCT03433781). This evidence concerns the gene TET2 and hematologic disorder.