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Résumé : The rhizobia-legume nitrogen-fixing symbiosis begins when plants perceive rhizobial Nod factors (NF), activating the Common Symbiosis Signalling Pathway (CSSP) that drives nodule organogenesis. Rhizobia also inject Type III effectors (T3E) into host cells through a Type III Secretion System (T3SS) related to those of pathogenic bacteria. These effectors were long viewed only as suppressors of plant immunity and determinants of host compatibility, but this picture has changed. Recent studies revealed that rhizobial effectors (known as Nodulation Outer Proteins, Nops) such as NopT, NopM, NopL, NopP and NopZ directly target NF receptors or associated kinases, thereby regulating CSSP activation. The effector-triggering nodulation proteins (ET-Nods), a separate class of T3Es found in various Bradyrhizobium species, can activate nodule organogenesis independently of NF perception by rewiring host transcriptional and SUMOylation-based signalling. We trace the evolutionary origins of these activities, which may derive either from redirection of ancestral immune-targeting effectors toward symbiotic functions or from rhizobium-specific innovations. We ask whether the T3SS contributed to nodulation. We then consider what this interference means for the host, ranging from reinforced partner choice to partial loss of host control, and argue that rhizobial effectors have evolved as specialised modulators that converge on the signalling hubs governing symbiosis.