This conclusion is supported by: (i) absence of personal/family history indicating hereditary cancer syndromes; (ii) lack of BRCA2 abnormalities in the initial 2015 tumor specimen, with deletion first detected after multi-line TKI therapies; and (iii) co-deletion of multiple HRR genes (RAD54L, FANCM, RAD51B, RAD51), suggesting genomic instability-driven somatic evolution. This evidence concerns the gene RAD51B and Inherited cancer-predisposing syndrome.