Taken together, these findings support the notion that meningitic E. coli infection induces the upregulation of and subsequent ADAM17-mediated proteolysis and secretion of HB-EGF, which results in the ligand-dependent EGFR transactivation as well as heterodimerization of EGFR–ErbB3, thus facilitating bacterial invasion of hBMECs. The gene discussed is EGFR; the disease is escherichia coli infection.