The result of its interaction is reported to be the reduction in DC activation and capabilities, as it halts the production of the costimulatory molecules CD80 and CD86 and activates the Wnt/catenin that stands as an obstacle to the stimulation of basic leucine zipper transcription factor ATF-like 3 positive (BATF3+) DC cells and renders the tumor resistant towards anti-PD1 treatment courses, despite the enhancement of PD-L1 expression. This evidence concerns the gene PDCD1 and neoplasm.