We will continue to utilize our in vitro model system for HPV16-mediated transformation and progression, which shares many gene expression changes with those found in premalignant cervical lesions and cervical cancer [44] to explore why HKc/DR are no longer responsive to the growth inhibitory effects of TGF-β1, even though substantial Smad signaling remains. This evidence concerns the gene TGFB1 and cervical cancer.