WNT3A and neoplasm: The proliferative activity is often co-opted by cancer cells, acting via transcriptional transactivation of proto-oncogenes such as MYC and CCND1. In the case of neuroblastoma, Wnt signalling has been proposed to be an oncogenic driver of MYC over-expression in non-MNA tumours [24], although our previous work did not detect significant increases of c-MYC or MYCN protein after Wnt3a/Rspo2 treatment of neuroblastoma cell lines [26].