Using a preclinical model of prostate cancer, the TRAMP-C2 model, the cluster regulatory interspaced short palindromic repeats (CRISPR)/Cas9-mediated deletion of Rab27a and PD1l, thus inducing exosomal PD-L1 loss, has proven that exosomal PD-L1 is involved in in vivo tumor growth, even at distant sites [128]. This evidence concerns the gene CD274 and neoplasm.