The molecular subtypification of the progesterone receptor (PR), estrogen receptor (ER), and HER2 status coupled with the histopathological classification (noninvasive or “in situ” carcinoma and invasive or infiltrating carcinoma) generates five different subtypes: luminal A (ER+ and/or PR+, HER2-, or low Ki67), luminal B (ER+ and/or PR+, HER2+, or HER2- with high Ki67), HER2-enriched (ER-, PR-, or HER2+), basal-like (ER-, PR-, HER2-, cytokeratin 5/6+, and/or HER1+), and normal-like (ER+ and/or PR+, HER2-, low Ki67, prognosis slightly worse than luminal A) [5–7]. The gene discussed is MKI67; the disease is in situ carcinoma.