We analyzed the potential druggability of somatic tumor variants identified in both patients in the context of somatic cancer evolutionary status, focusing on exonic and splice site variants with predicted protein-altering effects, copy number gains, and homozygous losses observed in the DNA (with the exception of TP53, for which we considered loss of heterozygosity to be potentially druggable) (Additional file 3 (Excel Doc B): Tables S8 and S9, Additional file 1: Supplementary Results). Here, TP53 is linked to cancer.