Expanding the RAS-verse: Novel Inhibitors, Emergent Dependencies, Fresh Opportunities in RAS-Mutant NSCLC.

Two studies in non-small cell lung cancer establish KRASG13C as a directly targetable oncoprotein and show codon 13-mutant tumors depend on wild-type RAS.

• Why it matters: Targeting KRAS has been difficult, and resistance or reliance on other RAS signaling can limit durable responses in NSCLC.
• What they did: The work combines direct KRASG13C targeting with analyses of how codon 13-mutant NSCLC relies on wild-type RAS, alongside testing for enhanced sensitivity to standard-of-care chemotherapy.
• The result: A third study shows that acquired oncogenic kinase fusions can rewire signaling through wild-type RAS, creating a therapeutically tractable resistance mechanism to KRASG12C inhibitors.

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