Overexpression of TGF-β (TGF-β1, TGF-β2, and TGF-β3) in ovarian cancer activates a TGF-β receptor/Ras-Related C3 botulinum toxin substrate 1 (RAC1)/Smad-dependent signaling pathway [36, 37] and in cervical cancer activates mitogen-activated protein kinases (MAPK), Smad, Wnt, tumor necrosis factor-α (TNF-α), and nuclear factor-κB (NF-κB) pathways [2, 38], promoting EMT. This evidence concerns the gene RAC1 and ovarian carcinoma.