KRAS mutation represents the most prevalent genetic mutation in NSCLC and serves as a pivotal driving factor in the pathogenesis of NSCLC.[37] Despite the gradual development of KRAS inhibitors, clinically targeted therapies against KRAS have not demonstrated prominent efficacy.[38] Additionally, Alternative strategies for targeting KRAS have been constrained by adverse effects resulting from non‐specific engagement with WT KRAS.[39] Thus, a better understanding of RAS signaling results in the creation of potentially effective inhibitors for KRAS‐mutant tumors. This evidence concerns the gene KRAS and non-small cell lung carcinoma.