The exploration of the cytoprotectiveeffects of autophagy in breast cancer cells subjected to the pharmacologically mediated depletion ofgrowth factor receptor signaling by mono-HER1 (i.e., gefitinib, cetuximab),mono-HER2 (i.e., trastuzumab), and dual HER1/HER2 (i.e.,lapatinib) inhibitors has confirmed that enhanced autophagic activity can contribute to moreefficient maintenance of cancer cell resistance to HER targeting drugs [48-51]. The gene discussed is EGFR; the disease is breast cancer.