In plants, guard theory is also known as indirect recognition.[5] This is because rather than direct recognition of a virulence factor or pathogen, there is instead recognition of the end result of a process mediated by a virulence factor or pathogen.[6] In these cases, the virulence factor appears to target an accessory protein that is either a target or a structural mimic of the target of that virulence factor,[7] allowing for plant defences to respond to a specific strategy of pathogenesis rather structures that may evolve and change over time at a faster rate than the plant can adapt to.[8] The interaction between pathogen and accessory protein results in some modification of the accessory protein, which allows for recognition by plant NBS-LRR proteins, which monitor for infection.[9] This model is best illustrated by RIN4 protein in A. thaliana.[10] RIN4 forms a complex with the NB-LRR proteins RPM1 and RPS2.[11][12] Protease effector AvrRpt2 is able to degrade RIN4, causing de-repression of RPS2.[13] On the other hand, AvrB or AvrRPM1-mediated phosphorylation of RIN4 results in activation of RPM1.[14] In short, this example elucidates how one NBS-LRR protein is able to recognize the effects of more than one virulence factor or effector.[15]