Ex vivoTumour-derived MVs were efficiently captured by DCs, stimulated DCs via cGAS/STING signaling → activation of type I IFN production by DCs → DC maturation and presentation of tumour antigens to T cells.In vivoH22 hepatocarcinoma, B16 melanoma, CT26 colon carcinomaVaccination (SC) of mice with microvesicles (MVs) activated protective immune response against tumours.Vaccination (SC) of mice with DCs loaded with MVs activated efficient antitumour therapeutic response.MVs were more immunogenic in comparison with exosomes. The gene discussed is STING1; the disease is melanoma.