Genomic enrichment analysis and mass spectrometry-based phosphoproteomics revealed that induction of EMT promotes resistance to KRAS inhibitors in a cell type-dependent manner through activation of PI3K/AKT or ERK pathways in NSCLC cells and co-suppression ERK or PI3K with KRAS(G12C) may prolong therapeutic benefit [38]. Here, KRAS is linked to non-small cell lung carcinoma.