In this study, we show that (a) blockade of PAK1 expression or activity in vitro down-regulates the expression of FA/BRCA pathway genes, (b) knock down or pharmacological inhibition of PAK in PAK1 overexpressing cells, compromises the ability of these cells to form Rad51 foci, (c) loss of PAK function reduces cell survival and promotes apoptosis, (d) PAK inhibition in PAK1 overexpressing breast cancer cells, sensitize these cells to PARP inhibition, and (e) small molecule inhibitors of PAK and PARP have a synergistic effect in vitro, and impair tumor growth in a xenograft setting. The gene discussed is PARP1; the disease is breast cancer.