SDCBP and breast carcinoma: 2016; Krishn et al. 2019). Hence, we tested the dependence of sEV‐induced cancer cell migration on EV uptake. Our data, however, argue for the hypothesis that cancer cell motility on sEVs predominantly relies on adhesive interactions between cells and vesicles independent of EV uptake. Furthermore, despite reports about sEV‐associated Integrin‐αVβ3 as a regulator for EV incorporation into recipient breast cancer cells (Altei et al. 2020), we observed no decrease in the uptake of Integrin‐αVβ3‐deficient Syntenin KO sEVs into above‐seeded cancer cells.