Although, Wang et al., demonstrated that PI3K and MAPK pathways were activated following anti-PD-1 therapy in NSCLC cells in vitro and in vivo, their study also showed that PD-1/PD-L1 dysfunction did not activate mTOR, illustrating that the mechanism behind tumor-intrinsic PD-1 to either induce or inhibit tumor growth may be different. The gene discussed is MTOR; the disease is non-small cell lung carcinoma.