In this context, the HDAC inhibitors (HDI) of the hydroxamate class Trichostatin-A (TSA) and Vorinostat (suberoylanilide hydroxamic acid; SAHA) have been demonstrated to promote a proteasome-dependent depletion of TCF4 levels in colon cancer cells; thus, significantly affecting their proliferation and viability [15]. Here, TCF4 is linked to colonic neoplasm.