Moreover, the inhibition of cancer cell proliferation by SeL may occur by suppressing NF-κB DNA binding [25], inhibiting protein kinase C (PKC) [7,29] or histone deacetylases (HDAC) [6,32] activity, as well as poisoning topoisomerase II (by reacting with thiols incorporated into this enzyme) [31] or by affecting other molecular targets, i.e., p38 mitogen-activated protein kinase (p38MAPK), c-Jun NH2-terminal kinase (JNK), AP-1 [3,7,26], ATM [31], AKT [7,26]. This evidence concerns the gene HDAC9 and cancer.