Earliest studies by Rao et al. and Burns et al. used multiplex PCR to detect CDKN2A deletion in brain tumors and correlated it with p16 expression in astrocytomas, where a strong correlation was found between p16 negative tumors and homozygous loss of CDKN2A [23]; as well as in glioblastomas, where diffuse p16 immunostaining was found to confidently exclude CDKN2A deletion but p16 immunonegativity did not always correlate with CDKN2A deletion [24]. This evidence concerns the gene CDKN2A and glioblastoma.