Class I and class IIb HDACs have been shown to be over-expressed in human colorectal cancer cells [18, 19], and these two HDACs may contribute to the regulation of cancer cell proliferation, differentiation, and apoptosis by either epigenetic or non-epigenetic modification to modulate p21, p27, cyclins, death receptors or proapototic proteins (e.g. Bim, Bax and Bak) expressions [20–26]. The gene discussed is BAX; the disease is colorectal cancer.