However, drug resistance may also depend on network adaptation mechanisms, including facilitation of resistance by feedback mechanisms (e.g., multiple feedbacks present in the MAPK pathway) [58], or activation of parallel pathways that bypass inhibition (e.g., amplification of MET or HER2 in NSCLC treated with EGFR inhibitors; and crosstalk between estrogen receptor and HER2 pathways in breast cancer) [56,57,59]. This evidence concerns the gene ESR1 and breast carcinoma.