Then, because STAT5a/b has been connected to DNA repair in chronic myeloid leukemia (CML) and it is a transcriptional regulator of RAD51 (22, 23), we have explored the possibility that STAT5a/b could be a potential target of iPA in glioblastoma cells. The gene discussed is RAD51; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.