Strategies for targeting KRASm NSCLC. Represented is canonical KRAS signaling. In its inactive state, KRAS is bound to GDP. Following activation of membrane receptors, KRAS bound GDP is exchanged for GTP resulting in KRAS activation. KRAS subsequently activates downstream signaling pathways such as the MAP/ERK and PI3K/AKT pathway leading to cellular proliferation and survival. Mutant KRAS as well as upstream and downstream effectors of the KRAS pathway are targets for small molecule inhibitors. Strategies to activate the anti-tumor immune response includes immune checkpoint inhibitors, engineered T cells expressing KRASm TCRs, and mRNA vaccines expressing KRASm neoantigens.

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