Other possible mechanisms involved in the compensatory interaction between the investigated pathways are HER2 phosphorylation at Thr701 and the interaction between HER2/EGFR and clathrin binding (55), as well as adaptive changes in the MAPK scaffolding proteins (KSR-1, GEF-H1) and receptor tyrosine kinases (MET, EGFR), leading to enhanced PI3K/AKT signaling in KRAS-mutant lung adenocarcinoma cell lines as revealed by mass spectrometry-based phosphoproteomics (33). This evidence concerns the gene KRAS and lung adenocarcinoma.