Compared to other inhibitors that globally affect nucleocytoplasmic shuttling, PSPC1-CT131 selectively affected the subcellular localization switch to sequester PTK6 in the nucleus, suppress PSPC1-mediated tumor progression, sustain cytoplasmic expression of inactive β-catenin and abolish downstream autocrine signaling of TGF-β1 and Wnt3a, which act in concert to mediate tumor suppression. The gene discussed is PSPC1; the disease is neoplasm.