The additive model did not show enrichment in DNA repair ontologies, but was significantly enriched in ontologies related to chromosome segregation during mitosis (p = 3.6×10−6) (Table 3 and Table S30 in File S1), driven by the genes KIF25[30], PINX1[31] and FANCA. A full GWAS using an additive model did not show any associations with genome-wide significant findings for any of the cancer mechanistic phenotypes (Figure S3). The gene discussed is PINX1; the disease is cancer.