CSCs secrete transforming growth factor-β (TGF-β) or upregulate its signaling which interferes with DCs antitumor responses by several mechanisms including (i) the reduction of mature DCs, or enhancement of the populations of tolerogenic DCs or DCregs [10], (ii) downregulation of MHC class II and DCs-costimulatory molecules (i.e., CD80 and CD86) [11], (iii) inhibition of CD103+DCs recruiting to the tumor site in Wnt/β-catenin-dependent pathway [12], and (iv) the development of PD-L+ DC impairing CD8+T cell activity or rising the resistance to anti-PD1 treatment [13]. Here, PDCD1 is linked to neoplasm.