Although pediatric cancers exhibit a lower tumor mutational burden than that of adult cancers, numerous pediatric cancers display genetic alterations or aberrant expression patterns of epigenetic modifiers involved in development and differentiation.8,23 Such mutations can alter normal developmental trajectories, thereby blocking differentiation.24 A notable example commonly observed in AT/RTs is a loss-of-function mutation in the SMARCB1 gene, which is a component of the mammalian SWI/SNF (mSWI/SNF) chromatin-remodeling complex.25,26. Here, SMARCB1 is linked to neoplasm.