This phenomenon, documented in a minority of AT/RT cases, may be explained by several mechanisms: 1) large genomic deletions or complex rearrangements not reliably captured by conventional targeted sequencing; 2) epigenetic silencing, such as promoter hypermethylation, requiring dedicated methylation assays for confirmation; and 3) tumor heterogeneity, where the tissue sample used for DNA extraction may have contained INI1-negative but SMARCB1 wild-type tumor cells (17, 18). Here, SMARCB1 is linked to neoplasm.