In all, this study supports other recent findings [23–28, 32] for the role of p16 as a surrogate marker of CDKN2A loss, and establishes a cutoff p16 value of 5% for detecting homozygous CDKN2A deletion with robust sensitivity and specificity, and a cutoff p16 value of 20% for excluding homozygous CDKN2A deletion, in both low and high-grade gliomas. This evidence concerns the gene CDKN2A and central nervous system cancer.