NGS and IHC analyses of the tumor revealed multiple defects in DDR genes and proteins, specifically, heterozygous truncating mutations in CHK1, FANCM, RAD50, POLD1, and FANCP; compound heterozygous truncating mutations in ARID1A; and loss of ATM and ARID1A protein by IHC. This evidence concerns the gene POLD1 and neoplasm.