Somatic duplications of the notochordal transcription factor brachyury (47, 48), chromosomal copy loss of phosphatase and tensin homolog (PTEN) (49), tuberous sclerosis complex (TSC) (50), cyclin-dependent kinase inhibitor 2A and 2B (CDKN2A and CDKN2B) (51), SMARCB1 (49), and PIK3CA (9) mutations are key aspects of chordoma pathogenesis, and therefore potential targets. This evidence concerns the gene CDKN2A and chordoma.