For all breast cancers combined, the final full model including 19 CNIs, clinical covariates, and tumor marker-approximated subtypes (estrogen receptor [ER], progesterone receptor, ERBB2 amplification, and Ki67) significantly outperformed a model containing only clinical covariates and tumor subtypes (C-Index full model, train[test]  =  0.72[0.71] ± 0.02 vs. C-Index clinical + subtype model, train[test]  =  0.62[0.62] ± 0.02; p<10−6). This evidence concerns the gene MKI67 and breast carcinoma.