The technology now exists to advance the concept of personalized medicine for all cancer patients. The advent of next generation sequencing can allow us to potentially characterize each individual's tumor for oncogenic driver mutations. It is unknown at present if a wide range of mutations in the phosphatidylinositol 3-kinase (PI3K) pathway predict for responsiveness to a PI3K inhibitor as would be expected in a situation of "oncogene addiction". In this study, we plan to explore two cohorts of patients and response to BYL719, an oral selective PI3K-alpha inhibitor: 1. Metastatic triple negative breast cancer (triple negative breast cancer [TNBC] which is defined as ER-/HER2-) and 2. PI3K pathway abnormal metastatic luminal breast cancer (ER+/HER2-). Both cohorts are eligible for this study after progression after standard first line therapy. In recent large sequencing efforts, for example The Cancer Genome Atlas [TCGA], primary breast cancers were found to have a large number of Pi3K pathway abnormalities- in TNBC there was a high rate of genetic abnormalities in the Pi3K pathway (combined mutations, amplifications and deletions in nearly 100% of TNBC)- as well as in ER+/HER2- disease. Therefore, in this study we plan to study responses to BYL719 and associations with genetic features that could signify Pi3K pathway activation in a cohort of fully molecular- characterized metastatic breast cancers in order to identify biomarkers of response to selective PI3K alpha inhibition in breast cancer.