In V. cholerae bacteria, the HapR regulator represses the expression of virulence genes. HapR expression is usually inhibited by the transducer protein LuxO, so that the bacteria are virulent. But V. cholerae emit two types of signal molecule that inhibit virulent behaviour in nearby V. cholerae bacteria. One of these, AI-2, is recognized by the LuxP receptor on the bacterial cell membrane. LuxP activates the LuxQ protein inside the cell, which deactivates the transducer protein LuxU. This prevents activation of LuxO, so that HapR activity is increased and virulence is suppressed. Higgins et al.4 show that the second signal molecule used by V. cholerae is 3-hydroxytridecan-4-one. This signal interacts with a putative receptor on the cell membrane (CqsS) that then deactivates LuxU, triggering the same signalling cascade described for AI-2 and LuxPQ.