In the extracellular space, PAMPs, DAMPs, or apoplastic effector proteins released from pathogens are recognized by cell surface membrane-bound receptors, inducing PTI. To suppress PTI, bacterial pathogens inject effectors into the host cell through a type-III secretion system, while fungi and oomycetes develop specialized structures such as haustoria to deliver effectors. Intracellular NLR receptors recognize specific effectors and trigger ETI, which is often associated with cell death at the infection sites. ETI can potentiate PTI by up-regulation of the underlying genes, while activation of PTI can enhance the defense response triggered by ETI. PTI and ETI work together to provide robust effective resistance against pathogens.