The use of flow-sorted tumor populations for CNV analysis enabled the identification of known driver lesions, including high-level focal amplicons targeting EGFR, JAK2, AKT2, MYC, and FGFR2, as well as homozygous deletions of both well-established PTEN, CDKN2A, ARID1B, GRB10, BRIP1, JAK1, and RB1, and unique RBM9, CEBPG, and EIF4G3 TNBC tumor suppressor genes. The gene discussed is ARID1B; the disease is neoplasm.