Tominaga et al. showed that miR-181c in EVs derived from breast cancer cells contributes to breaking the blood–brain barrier through the abnormal localization of actin via the downregulation of the miR-181c target gene, PDPK1, which leads to the downregulation of phosphorylated cofilin and the resultant activated cofilin-induced modulation of actin dynamics [43]. The gene discussed is CFL1; the disease is breast carcinoma.