The virulence-enhancing effects by φRSS1 infection can be explained as follows: surface-associated φRSS1 particles (or phage proteins) may change the surface nature (hydrophobicity) of host cells to generate a high local cell density, resulting in early activation of phcA, the global virulence regulator, or lack of orf13, which is absent from the φRSS1 genome (Addy et al., 2012b). Here, ACER3 is linked to infection.