Both typical Rho GTPases (RhoA, RAC1 and Cdc42 which cycle between an active GTP-bound and inactive GDP-bound conformation and are regulated by GEFs (guanine nucleotide exchange factors), GAPs (GTPase-activating proteins), and GDIs (guanine nucleotide dissociation inhibitors)) and atypical Rho GTPases (GTPase-deficient mutations and those that generally do not hydrolyze GTP) contribute to cancer progression. This evidence concerns the gene RAC1 and cancer.