PIK3CA and non-small cell lung carcinoma: Consistent with this, silencing of PD-1 or therapeutic antibody blockade of PD-1 on the surface of NSCLC and colorectal cancer cells increased proliferation in vitro via activating PI3K and MAPK pathways (15), suggesting that PD-1 could be involved in development of resistance to immunotherapy blockade in NSCLC and could provide one explanation for why patients with NSCLC can display hyperprogressive disease following treatment with anti-PD-1 therapy (15, 203).