Mechanisms driving cell proliferation are often conserved between development and tumorigenesis, so it is not surprising that in SHH medulloblastoma, the same mitogenic pathway responsible for development of the cerebellum is aberrantly activated through mutations of regulators (PTCH1, SMO, SUFU) or amplification of downstream effectors (MYCN, YAP1, GLI)3,5. This evidence concerns the gene YAP1 and medulloblastoma.