An example of this dichotomous response to IL17A has been shown in K-ras vs. non-K-ras models of NSCLC, where IL17A was shown to promote growth in K-ras-driven tumors (10), but IL17A were required to inhibit early oncogenesis in a non-K-ras driven model (11). The gene discussed is KRAS; the disease is non-small cell lung carcinoma.