Consistent with previous findings from preclinical studies of breast [17, 23] and prostate cancers [19], we also found that suppression of the PI3K signaling by BKM120 was accompanied by increased abundance of the double-stranded break marker γ-H2AX and decreased abundance of homologous recombination (HR) repair protein RAD51 in well-established cell models of PIK3CA mutant ovarian cancer. The gene discussed is H2AX; the disease is Familial prostate cancer.