Data herein presented regarding the role of WT1 as a repressor of ZNF224 gene in CML could also contribute to explain the mechanism leading to ZNF224 induction by ara-C and the consequent apoptosis; indeed, our previous observation that ara-C induces a down-modulation of WT1 in K562 cells [13] correlates well with the ZNF224 up-regulation that we found following treatment with either ara-c or imatinib. The gene discussed is ZNF224; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.