Indeed, we provide support for the notion that both HDACi and MTM promote neuroprotection by inhibiting the expression or functions of proteins that mediate transformation such as Myc, HDAC1, HDAC2 and HDAC3 [2,10-13] and by promoting the expression of tumor suppressors such as p21waf1/cip1. The gene discussed is CDKN1A; the disease is neoplasm.