Further, the number of Granzyme B and CD69 double positive CD8+ T cells as well as Granzyme B and IFNɣ double positive CD8+ T cells were found to be significantly higher in the antagomiR-182-5p treated group (Fig. 5o), suggesting that reprogramming macrophage plasticity by inhibition of exosomal miR-182-5p may serve to activate resident CD8+ T cells, thereby enabling efficient tumor cell killing. Here, CD69 is linked to neoplasm.