Combining all detected homozygous deletions, focal amplifications and validated somatic nucleotide substitutions, they found three major pathways affected in a high percentage of glioblastomas: receptor tyrosine kinase signaling (altered in 88% of the GBMs), TP53 signaling (altered in 87%) and the pRB tumor suppressor pathway (altered in 78%). Here, RB1 is linked to glioblastoma.