Several mechanisms of effector-triggered immune responses have been proposed in plants, including two well-studied models. a, In the ‘gene-for-gene’ model, a pathogen avirulence (Avr) protein directly interacts with a host resistance (R) protein. This interaction activates a subsequent immune response from the host. b, In a second model, the guard model proposes that host proteins ‘guard’ cellular processes, and the disruption of these processes by virulence factors can be sensed by the host. For example, a pathogen effector that modifies a host protein can trigger recognition of this modification by the host cell, which then initiates an immune response. Since the activity of the effector, rather than the effector itself, is detected, this model of ETI does not rely on direct effector recognition.