Recent work from several labs have shown ARID1A, the helicase/ATPase-containing SWI/SNF chromatin-remodeling factor, to be mutated in several cancers, most notably in ovarian cancer (some 50% of ovarian clear-cell carcinoma). Other cancers in which ARID1A was reported to be mutated include Sézary syndrome (a leukemic form of cutaneous T cell lymphoma; ~26%), pancreatic cancer (~25%), breast cancer (~23%), Waldenström macroglobulinemia and Burkitt lymphoma (~17%), stomach cancer (~16%), bladder cancer and liver cancer (~13%), colon cancer (~10%), mantle cell lymphoma (~9%), prostate cancer (~8%), lung cancer (~6%), and medulloblastoma (~2%). ARID1A mutations were also detected in few cases of extranodal natural killer (NK)/T-cell lymphoma (NKTCL) and acute lymphoblastic leukemia (ALL). While ARID1A is currently not druggable, synthetic lethal screens have uncovered molecular drug targets such as the histone methyltransferase EZH2 and the Src family tyrosine kinase YES1. Thus, in ovarian cancer, targeting EZH2 with the GSK126 EZH2-inhibitor or with the YES1-inhibitor Dasatinib, inhibits tumor growth in a mutant ARID1A-depend manner, indicating a possible tumor-targeted (or “personalized medicine”) approach for mutant ARID1A cancers (Cancer Epigenetics Society news; November 17, 2016).