AKT1 and ovarian cancer: Dorayappan et al. showed that hypoxic ovarian cancer cell-derived sEVs were proficient in significantly decreasing dsDNA damage and increasing cell survival in response to cisplatin treatment [66], while Zhu and colleagues found that sEVs from hypoxic macrophages can promote in vitro and in vivo chemoresistance in ovarian cancer cells, through the vesicular miR-223/PTEN-PI3K/AKT pathway [74].