In fact, ROS production was implicated in DNA damage observed in U87-MG and U251-MG cells, but not in LN229, indicating that other molecular alterations may participate, such as alteration of the DNA-repair machinery,19 the acetylation of histones involved in DNA repair such as Histone 427 or histone 328 and the decrease in G2 checkpoint kinases.22 Our results show that HDACi display at least two of these effects on glioma cells, as they decrease the expression of G2 checkpoint kinases Wee1 and Chk1 and DNA damage repair protein Rad51. This evidence concerns the gene WEE1 and central nervous system cancer.