H2AX and glioblastoma: As shown in Fig. 2a, as expected seen the key role of SETD8 in orchestrating DNA damage response [7], SETD8 inhibition resulted in an even greater increase of DNA damage in all the treated glioblastoma cell lines, as demonstrated by the significant high number of p-γ-H2AX foci in both proficient- and deficient-p53 cells.