Mechanistically, high level of ANXA3 released by CAFs has been confirmed to activate the JNK/survivin pathway in both cell-line models (A549, H661 and SK-MES-1) and mouse xenograft models of NSCLC, resulting in a markedly attenuated IC50 of cisplatin in vitro and an augmented xenograft tumor growth under cisplatin exposure in vivo (Wang et al., 2019). The gene discussed is BIRC5; the disease is neoplasm.