Targeted NGS ctDNA assays are warranted to manage the complexity of genomic alterations; however, intrinsic and acquired resistance also involves the identification of pathways that influence sensitivity, such as in KRAS G12C‐mutant NSCLC, where the combination of the KRAS G12C inhibitor, PI3K inhibitor, and SHP2 inhibitor caused tumor regression in mouse models with acquired resistance to AMG510 [111]. Here, KRAS is linked to neoplasm.