The hypersensitive reaction (HR) in plants is characterized by locally induced cell death in the presence of pathogen effectors to contain the spread of the microorganism. This HR depends on a network of NLR receptors that specifically interact with the effector and communicate the signal to NRC proteins, which are responsible for cell death by forming an oligomer (or resistosome) that inserts into the membrane, disrupting ion homeostasis. The plant-pathogenic nematode Globodera rostochiensis produces effectors of the SPRYSEC family, one of which (SPRYSEC15) directly binds to and inhibits the activity of NRC2 and NRC3, which act downstream of the receptor. This implies that the gene-for-gene evolutionary model of the effector-receptor interaction can extend to other members of this immune system, imposing selective pressure on the host to prevent interaction. In this work, we analyze the evolutionary history of the interaction between SPRYSEC15 and NRC3.