In contrast, Moorhead and Griffiths (2011) found that C. jejuni could respond to quorum-sensing (QS) signaling molecules (such as C4-HSL, 3OH-C4-HSL, C12-HSL, and HSL), which indicated that biofilm formation was blocked and the entry of cells into the VBNC state was delayed. It was speculated that QS signaling molecules were related to formation of the VBNC state. This conjecture was further confirmed by Ayrapetyan et al. (2014), who only found that the QS signaling molecule autoinducer-2 (AI-2) could directly awaken the VBNC cells of V. vulnificus but also that the AI-2 deletion mutant lost resuscitation ability from the VBNC state. Bari et al. (2013) also demonstrated that the resuscitation of dormant V. cholera was dramatically improved by the addition to the enrichment medium of biologically synthesized AIs, suggesting that these molecules might signal to dormant cells and then improve conditions for better growth. Furthermore, rpoS deletion mutant strains could not be resuscitated even with the addition of exogenous AI-2. This result shows that RpoS is not only a significant protein for VBNC formation but also an important participant in the resuscitation process mediated by AI-2.