Although these studies have focused on synthetic lethal interactions involving inactivation of SWI/SNF activity in solid tumors, particularly in ovarian cancers, which exhibit high mutational frequencies of ARID1A, similar strategies can be extended potentially to hematological malignancies harboring mutations of ARID1A. For instance, in APL cases with mutation of ARID1A, standard therapy (either ATRA or arsenic trioxide) could be combined with an approach directed at ARID1A deficiency, thus leading to potentially improved and personalized therapeutic approaches. The gene discussed is ARID1A; the disease is hematologic disorder.