The expression of ER, PR, HER-2, and Ki-67 have been used to discriminate different molecular subtypes (Luminal A, Luminal B, HER-2-enriched, and Triple-negative).[26] Similar molecular phenotypes seen in invasive cancer presented in primary DCIS using immunohistochemistry surrogate markers.[27,28] Patients with DCIS with microinvasion in our study were significantly more likely to have HER-2-enriched and Triple-negative tumors or less likely Luminal A and Luminal B type tumors than patients with DCIS. This evidence concerns the gene ERBB2 and ductal breast carcinoma in situ.