We have shown that tyrosyl phosphorylated PAK1 (pTyr-PAK1) facilitates PRL-dependent breast cancer cell motility via several mechanisms: formation of paxillin/GIT1/βPIX/pTyr-PAK1 complexes resulting in increased adhesion turnover and phosphorylation of actin-binding protein filamin A(Hammer, Oladimeji, De Las Casas, & Diakonova, 2015; Hammer et al., 2013; Rider & Diakonova, 2011). This evidence concerns the gene PAK1 and breast carcinoma.