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). Here, KRAS is linked to neoplasm.