Taking all these clues together, we therefore present our hypothesis and have evidenced that meningitic E. coli infection of hBMECs triggered ANGPTL4-mediated ARHGAP5/RhoA signaling, which increased MYL5 expression and finally led to the dysfunction of BBB, and this ANGPTL4–ARHGAP5–RhoA–MYL5 may present another way for meningitic E. coli penetration of the BBB. Here, MYL5 is linked to escherichia coli infection.