Inspired by our finding that GATA3 functions downstream of BRCA1 to suppress EMT in breast cancer [15] and that BRCA1 deficiency stimulates the expression of FRA1 in mammary tumors [38, 39], we hypothesized that reconstitution of GATA3 in BRCA1 deficient tumor cells also restores the expression of AP-1, thus inhibiting tumorigenesis. The gene discussed is FOSL1; the disease is neoplasm.