This incomplete penetrance as well as the late tumor onset may suggest that similarly to PAK1, PAK4 itself acts as a relatively weak oncogene and/or to facilitate tumor formation driven by other oncogene(s), the latter supported by the activating KRAS mutations that we observed in these tumors and the finding that PAK4 overexpression overcame RAS-induced senescence in mammary epithelial cells. The gene discussed is KRAS; the disease is neoplasm.