IL1B and infection: Indeed, based on our work focusing on CNF1 and studies of Salmonella typhimurium SopE/E2 virulence factors, we can speculate that the abnormal activation of Rac/Cdc42 triggers the assembly of an anti-virulence immune complex involving NOD1 and RIP kinases to promote NF-κB activation and in parallel to assemble a Rac/ASC/caspase-1 complex for the maturation of IL-1β during infections [27,35].