As PIK3CA has been shown to be activated through somatic mutation in >25% of colorectal, breast and ovarian carcinomas, as well as in human CNS tumors (including anaplastic oligodendrogliomas, glioblastoma multiforme and medulloblastoma), we hypothesized that PIK3CA mutations may substitute for activating RAS lesions in neuroblastoma tumourigenesis. The gene discussed is PIK3CA; the disease is glioblastoma.