Using a mouse model of K-RAS gene-induced lung cancer, Felix et al. found that IL-17C-mediated innate inflammatory responses enhance cancer cell resistance to anti-programmed cell death protein 1 (PD-1) immunotherapy, and that blocking the IL-17C signaling pathway may improve the outcomes of patients with lung cancer receiving PD-1 therapy.323 Similarly, Esra et al. showed that blocking IL-17 is an effective method for improving PD-1 therapy efficacy.324 Many clinical studies have indicated the role of IL-17 in tumors and the efficacy of anti-IL-17 therapy (Table 2). The gene discussed is KRAS; the disease is lung carcinoma.