Indeed, substituting the N-terminal region of the infection-incompetent angiotensin II receptor AT1R with that of the human β2AR produced a chimeric receptor that could be activated by meningococci in vitro9, suggesting that some direct or indirect N. meningitidis interaction with the β2AR N-terminus might mediate β-arrestin-selective signaling. The gene discussed is ADRB2; the disease is infection.