By closing off two major pathways contributing to cancer cell proliferation and survival, the coupling of PI3K and G12C inhibitors provides a more broadly effective approach in comparison to coupling with a specific SHP2 or MEK/ERK inhibitor due to comparably better tolerance of PI3K monotherapy in patients with lung cancer as well as the fact that reactivation mechanisms under MEK/ERK inhibition are extremely variable [85, 107]. This evidence concerns the gene MAP2K7 and lung cancer.