In T cell leukemia cell lines, engineered overexpression of the poly-ADP ribose-degrading enzyme PARG, or siRNA-mediated knockdown of PARP1 and/or PARP2 expression and specific PARP inhibitors were used to show that PARP activity and/or sufficient poly-ADP ribose levels are necessary to maintain a transcriptionally permissive state at a TET1 CpG island, surrounding its transcription start site [226]. This evidence concerns the gene PARP1 and T-cell leukemia.