 Pre-clinical studies in cells and in mice show that synthetic lethality for deficient "ARID1A" expression occurs by either inhibition of the methyltransferase activity of EZH2, by inhibition of the DNA repair kinase ATR, or by exposure to the kinase inhibitor dasatinib.There are two pathways for homologous recombinational repair of double-strand breaks.The major pathway depends on BRCA1, PALB2 and BRCA2 while an alternative pathway depends on RAD52.