The concept of immunoediting suggests that the immunity boosted by anti-PD1/PDL1 therapy not only protects the host against tumor progression but also results in selection of tumor subclones that can escape antitumor immunity, which ends up leading to the acquired resistance of anti-PD1/PDL1 therapy (Schreiber et al., 2011; Matsushita et al., 2012; O’Donnell et al., 2019). Here, PDCD1 is linked to neoplasm.