TGF-β1 was reported to act as a tumor suppressor during the early stages whereas cell proliferation and induction of a metastatic phenotype was prevalent during the later stages.[35] Moreover, in some but not all forms of cancer, PKCα protein expression was downregulated and in PKCα knockout mice spontaneous intestinal tumors were identified.[28] Thus, the TGF-β1 paradox identified during cancer progression may apparently extend to neonatal rat ventricular fibroblasts. This evidence concerns the gene PRKCA and cancer.