The development of DCIS generally begins through hereditary or acquired mutations that affect tumor suppressor genes (e.g., BRCA1, BRCA2) or oncogenic genes (e.g., HER2/neu), which disrupt cellular regulatory control and promotes unrestricted proliferation, resistance to apoptosis is enhanced (Solin, 2019). The gene discussed is ERBB2; the disease is ductal breast carcinoma in situ.