Specifically, we show that miR-150 in lung cancer-secreted EVs contributes to the aforementioned processes by: (1) reducing the expression of CD226 on NK cells; (2) creating a favorable immunosuppressive microenvironment by releasing IL-10 and S100A8 protein; and (3) exploiting angiogenesis in the TME via VEGF, CXCL1 and CXCL8 production. Here, CXCL1 is linked to lung carcinoma.