The patient is a 41-year-old premenopausal woman who discovered a lump in the upper outer quadrant of the left breast. The workup was conducted in July 2015 within a week of symptom onset. Bilateral diagnostic mammography revealed pleomorphic calcifications in the area of concern. An ultrasound revealed a 3.2-cm solid mass in the 2: 00 position 8 cm from the nipple, and 2 smaller masses in the 2: 30 position that were 4 cm from the nipple, which appeared to represent multifocal disease. An ultrasound-guided breast biopsy was performed. The 2: 00 o'clock lesion contained infiltrating duct carcinoma with intermediate- to high-grade features and duct carcinoma in situ (DCIS) with comedonecrosis. The 2: 30 lesion contained DCIS as well. The estrogen receptor (ER) stained 100%, and the progesterone receptor 12%. The HER2 FISH was 1.1. An MRI of the breast was performed which showed a suspicious lesion on the right side. A biopsy of the contralateral breast lesion was negative. The left axillary lymph nodes (LNs) were sampled by ultrasound-guided fine needle aspiration and were negative. Because the breast cancer was locally advanced by examination, a metastatic survey was undertaken. Metastatic disease was not discovered; however, a CT of the body revealed a 2.6-cm mass in the tail of the pancreas. The CA19-9 was 126 (normal 0–38). A positron emission tomography (PET) scan was positive in the pancreas with an SUV level of 3.6. A CT-guided biopsy of the lesion revealed adenocarcinoma. Immunostains for villin and CA19-9 were positive, and negative for ER, establishing pancreatic origin and ruling out the diagnosis of a metastatic lesion. The patient was taken to the operating room in August 2015 and underwent a left modified radical mastectomy. Pathology revealed a 7.5-cm grade 2 (tubule 3, nuclear 3, mitoses 1 = 7/9) infiltrating duct carcinoma with lymphovascular invasion. A component of high-grade DCIS with solid and cribriform features occupying 50–60% of the tumor and containing comedonecrosis was also identified. The deep margins for both the invasive and in situ components were clear by 0.6 cm and 8/23 LNs were found to contain metastatic cancer. She was considered to have a G2 pT3N2aM0, AJCC stage IIIA breast cancer. In September 2015, the patient underwent a laparoscopic, hand-assisted splenectomy, distal pancreatectomy, lymphadenectomy, and concomitant bilateral salpingo-oophorectomy. Pathology revealed a 3.2 × 2.3 × 2.0 cm moderately differentiated adenocarcinoma with invasion of the peripancreatic fat. Perineural invasion was present, but vascular invasion was not. The resection margins were 1.8 cm from proximal pancreatic margin; 1/13 regional LNs contained metastatic disease. She was considered to have G2, pT2N1M0, AJCC stage IIB pancreatic cancer. The fallopian tubes and ovaries were submitted entirely for microscopic examination and were histologically unremarkable. Germline genetic testing (Inherited Cancer Screen, Counsyl Inc., South San Francisco, Calif., USA) confirmed the presence of a deleterious BRCA2 mutation characterized as c.5681(dupA). Her father, who was diagnosed with prostate cancer at age 69, and her younger brother carry the same BRCA2 mutation. No mutations were identified in 23 other genes associated with hereditary cancer []. Genomic profiling was performed on both cancers (FoundationOneTM, Foundation Medicine, Inc., Cambridge, Mass., USA) employing hybrid capture, next-generation sequencing of DNA in the exomic regions of 315 genes. The results of this somatic analysis revealed the mutation Y1894fs*1, also known as c.5681(dupA) in both cancers, as well as a second BRCA2 mutation and a KRAS G12R mutation in the pancreatic cancer. Common genetic alterations of unknown significance in FAT1 and CREBBP genes were also identified in both the breast and pancreas cancers. The patient received genetic counseling. Adjuvant chemotherapy utilizing doxorubicin-cisplatin followed by gemcitabine-NAB paclitaxel was administered postoperatively. The patient will receive postmastectomy radiotherapy, upper abdominal radiotherapy, aromatase inhibitor therapy, and will be considered for olaparib therapy in view of her still ominous prognosis, despite the fact that she could not qualify for participation in a clinical trial with olaparib because of the exclusion of patients with two primary malignancies. The pedigree reveals a small kindred. The patient's father was diagnosed with prostate cancer at age 69. He was confirmed as carrying the same BRCA2 mutation as his daughter. The patient's brother, who is a decade younger, also carries the familial mutation, but so far has not been diagnosed with a malignancy at age 30. The paternal grandfather had lung cancer.