Evidence has emerged that pathogenic or commensal bacteria subvert the ubiquitin and ubiquitin-like pathways (ULPs) during interaction with their hosts. This finding is consistent with ULPs being important in signalling cascades that relay the cellular recognition of pathogens to trigger a genetic response by the host. Subversion of these pathways also contributes to the prevention of host-cell damage by limiting the intracellular activities of bacterial virulence factors. Given the growing implication of ULPs in cell signalling, autophagy and membrane trafficking, there is little doubt that further examples of direct or indirect interactions between bacterial factors and ULPs will be documented.