By contrast, NSCLCs harboring KRAS or BRAF mutations, which frequently arise in smokers, typically exhibit higher TMB and an “inflamed” tumor microenvironment, resulting in comparatively stronger responses to ICIs, reflecting the significant influence of smoking status on immunotherapy outcomes and underscoring the intricate interplay between genetic alterations and environmental factors, such as smoking, in shaping the immune landscape of oncogene-driven NSCLC. The gene discussed is KRAS; the disease is non-small cell lung carcinoma.