Given the prevailing theory that genomic instability produces neoantigens to elicit an adaptive anticancer immune response (1, 6, 19, 20), two key pathways are of interest: TP53 is the most frequently occurring mutation in breast cancer (11) and homologous recombination deficiency (HRD) occurs at increased frequencies in breast cancer, second only to ovarian cancer in a pan-cancer comparison (21, 22). Here, TP53 is linked to hypoparathyroidism-retardation-dysmorphism syndrome.