We speculate that as for RUNX2 in osteosarcoma,[32] the expression and/or function of FOXP2 in malignant cells may be frequently compromised, which may explain the lack of overt growth arrest phenotype and induction of p21WAF1/CIP1 in SH-SY5Y cells stably engineered to over-express recombinant FOXP2.[3, 4] Alternatively, FOXP2 may require one or more co-operating factors to initiate growth arrest in normal developing populations. Here, CDKN1A is linked to osteosarcoma.