In 4 T1 tumor models, the accumulation of exosomal PD-L1 in the tumor microenvironment induced immunotherapy resistance by suppressing the secretion of granzyme B. Notably, knockdown of Rab27a in tumor cells significantly enhanced the efficiency of anti-PD-1 therapy and inhibited 4 T1 tumor growth [71]. The gene discussed is CD274; the disease is neoplasm.