Studies suggested that EspH blocks Rho activation to antagonize bacterial phagocytosis (invasion) by macrophages.13 ABR has also been implicated in negatively regulating phagocytosis.33 Studies have also shown that while at an early infection time, EPEC-wt or EPEC-∆espH induce filopodium formation, EPEC-∆espH/pEspHwt strongly suppresses the filopodium formation.19,22 Given these observations, we asked whether the EspH-ABR interactions, shown to downregulate Rac1 and Cdc42, play a role in bacterial invasion and filopodium formation. The gene discussed is RAC1; the disease is infection.