able numbers of larger cells with a luteinized or rhabdoid appearance. Though the presence of follicle-like spaces is diagnostically informative, other nonspecific morphologic and immunohistochemical features render the diagnosis challenging to establish.[@cit0005] Indeed, until the discoveries outlined in this addendum, no specific immunohistochemical markers existed. Although SCCOHT is often diagnosed at an early stage, little evidence exists to support treatment selection and the prognosis is dismal with 2-year survival being less than 35%.[@cit0005] SCCOHT\'s early age of onset and aggressive clinical course clearly establish a pressing need for innovations in management of this disease.

Inactivating SMARCA4 Mutations in SCCOHT {#s0002}
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Prior to the discoveries described below, SCCOHT\'s molecular etiology was understood primarily according to its clinical pathology and expression profile. No mutations had been identified by targeted sequencing of candidate genes such as KRAS, BRAF, BRCA1, BRCA2, and TP53 and the genome was seen to be predominantly diploid by comparative genomic hybridization.[@cit0011] Now, next-generation sequencing analyses from independent laboratories have reframed our biological understanding of SCCOHT by revealing that nearly all tumors harbor inactivating, often bi-allelic, mutations in the chromatin-remodeling tumor suppressor gene SMARCA4.[@cit0001] We previously sequenced tumor or germline DNA from 12 SCCOHT cases and the patient-derived BIN-67 cell line, identifying inactivating mutations in 9 of these samples.[@cit0001] We also found 15 of 18 cases with loss of SMARCA4 protein expression by immunohistochemistry. We now report the SMARCA4 status of an additional 12 SCCOHT tumors, 3 matched germlines, and the cell line SCCOHT-1[@cit0014], bringing the total number of cases analyzed in our hands to 24. This analysis was performed by PCR amplification of all coding exons of the SMARCA4 gene using DNA extracted from formalin-fixed paraffin-em