CDKN2A and central nervous system cancer: It has been speculated, however, that the biological function of IDH mutation may be skewed by the inactivation of both TP53 and RB1 genes [10], as multiple studies have demonstrated that, in the absence of CDKN2A/B homozygous deletion, IDH mutation inhibited glioma genesis and extended survival in comparison with wild-type IDH [19,20,21].