However, as commonly found in several cases of cancers, whereby the tumor suppressor APC is not functional or the activity of GSK3β is diminished by the activation of Wnt signaling pathway, an excessive amount of β-catenin in the cytoplasm can migrate to the nucleus, where it functions as a cofactor for the transcription factor T-cell factor (TCF) and potentiates its transcriptional activity in concert with the activated SMAD 2 and 3, triggered by TGFβ signaling (Figure 1) [44]. The gene discussed is TGFB1; the disease is cancer.