Hyperprogression under anti-PD-1 mAbs has been reported also in patient with non-hematological tumors and several mechanisms have been implicated, including expansion of PD-1+ regulatory T cells (Tregs), compensatory up-regulation of alternative ICs, immunotherapy-related induction of cancer stem cells, reprogramming of tumor associated macrophage from M1 to M2 phenotype as a consequence of their binding to the Fc portion of the anti-PD-1 mAb (37). Here, PDCD1 is linked to neoplasm.