Despite the role of these pathways in apoptosis and proliferation of breast cancer cells, we did not include them in the model either because the literature we explored pointed to them behaving very similarly to a pathway included in the model (e.g., in the case of EGFR and FGFR), or because we were not able to find strong evidence linking them to the response/resistance to the targeted drugs studied (e.g., in the case of the DNA damage pathway). This evidence concerns the gene EGFR and breast cancer.