Prominent examples include malignant rhabdoid tumors, driven by biallelic loss of the chromatin remodeler SMARCB1, with few other recurrent genetic mutations [8,10], diffuse midline glioma (DMG), driven by oncogenic histone mutations, leading to altered histone methylation [11,12], and pediatric hindbrain ependymomas, which have a minimal mutational burden and, instead, are driven by altered DNA methylation [9]. Here, SMARCB1 is linked to rhabdoid tumor.