These mutations resemble recurrent mutations in other pediatric cancer types with HOX gene expression and immature phenotypes (MLLT1 p.C118QPPG in Wilms tumor57 or H3F3A p.K28M in high-grade glioma58), postulating a shared mechanism of tumorigenesis among these pediatric neoplasms. This evidence concerns the gene MLLT1 and childhood neoplasm.