Here we provided a unique BRCA1-mutant at-risk in vitro model and demonstrated an evidence that coordinated activation of PAF-PAFR, and FAK and STAT pathways, with the abnormal BRCA1 functions may contribute to the significant increases of malignant potential and early events of tumor transformation in at-risk ovarian epithelium (Fig 6E). The gene discussed is PTAFR; the disease is neoplasm.