The response that may induce drug resistance to these KRASG12C inhibitors can be divided into following categories, (i) mutations in KRAS, e.g., at G13, R68, H95, Y96, or multiple copies of KRASG12C; (ii) mutations in genes other than KRAS; (iii) Transitioning to other cancers, e.g., transitioning from adenocarcinomas to squamous cell carcinomas (66). This evidence concerns the gene KRAS and squamous cell carcinoma.