Using mouse models to establish mutational timing effects, the authors displayed that SMARCB1 loss in early neural crest cells was necessary to initiate tumorigenesis in the cranial nerves and meninges, leading to rhabdoid tumors, while SMARCB1 loss with concomitant NF2 LOF at a later developmental stage, in the Schwann cell lineage, led to a schwannoma [168]. The gene discussed is SMARCB1; the disease is rhabdoid tumor.