The phosphorylation of STAT1α by TGF-β1 leads to its activation and the dissociation of STAT1α from TβRII/ALK5 receptor complex that releases the blockage and, in turn, increases the phosphorylation of Smad2, executing TGF-β signal transduction in ovarian cancer cells. This evidence concerns the gene TGFBR2 and ovarian carcinoma.