In Case 1 of the present study, tumor cells progressing to SCC acquired BAP1 mutation close to a splice‐donor/acceptor consensus motif, which in the concurrent absence of a wildtype BAP1 allele (due to Chr 3p LOH), would be sufficient to accomplish homozygous loss‐of‐function and potentially contribute to subclonal tumor progression. This evidence concerns the gene BAP1 and neoplasm.