For example, although adagrasib can reverse multidrug resistance mediated by the MDR1 transporter (Zhang et al., 2022), the resistance to adagrasib has emerged through heterogeneous subclonal mutations in RAS-MAPK pathway components (e.g., NRAS, BRAF, and MAP2K1) that enable NSCLC tumor cells to reactivate MAPK signaling and bypass KRAS(G12C) inhibition (Tanaka et al., 2021). The gene discussed is KRAS; the disease is non-small cell lung carcinoma.