An example for this concept are cancers with homozygous loss of p16/CDKN2A resulting in the passenger deletion of the enzyme methylthioadenosine phosphorylase (MTAP) (which is found in ~15% of all cancers and>50% of glioblastoma multiforme) and inhibition of the enzyme arginine methyltransferase (PRMT5) (12–14). This evidence concerns the gene CDKN2A and glioblastoma.