AKT1 and urinary bladder cancer: It was demonstrated that exosomal miR-21 derived from bladder cancer cells could suppress phosphatase and tensin homolog (PTEN) of phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha/AKT (PI3K/AKT) signaling pathway and activate STAT3 expression to promote M2 phenotype polarization in macrophages [73], and miR-34a from triple negative breast cancer can promote M2 macrophage polarization through MCTS1 re-initiation and release factor (MCT-1)/miR-34a/IL-6/IL-6R signal axis [74].