In squamous cell carcinoma resistant to PI3K inhibitors, dimerization of AXL with EGFR activates the PLCγ/PKC/mTOR pathway to sustain tumor progression [61••], and in mesenchymal ovarian tumors and cell lines, AXL dimerized with MET, EGFR, and HER2, leading to sustained ERK activation [62•]. This evidence concerns the gene EGFR and ovarian neoplasm.