Despite significant advances in medicine, breast cancer (BC) remains a prominent and fatal cancer for women globally. On a molecular level, BC is driven by the amplification of ERBB2 expression, activation of hormone receptors such as estrogen (ER) and progesterone (PR) and BRAC mutations. Considering this mechanistic heterogeneity, the treatment of BC requires enhanced understanding of different metabolic pathways including ER, ErbB2, and PI3K/AKT/mTOR. In the Meiler Lab, we leverage state of art computational methods to understand the mechanism of activation induced by genomic alterations of the receptor protein HER2. We simultaneously apply computational modeling in collaboration with cellular studies to understand the mechanisms of resistance of HER2 mutants towards different drug targets.