The present study illustrates for the first time the specific and divergent effects of EVs-derived from different cell sources (human endothelial cells, adipocytes, monocytes and macrophages) following IH exposures, and their potential contributions to the adverse consequences commonly associated with OSA (i.e., vascular dysfunction, macrophage polarity changes, and insulin resistance). The gene discussed is INS; the disease is isolated hemihyperplasia.