Effector Triggered Immunity (ETI) is activated by the presence of pathogen effectors. Pyruvate kinase activity is most broadly regulated by allosteric effectors, covalent modifiers and hormonal control. Plants also carry immune receptors that recognize highly variable pathogen effectors. Allosteric enzymes are usually under the simultaneous control of several allosteric effectors. Several studies have also identified additional substrates that can act as allosteric effectors. They are responsible for the upregulation of innate immunity effectors, including antimicrobial agents and chemokines. This activates the effectors that in turn cleave other proteins resulting in apoptotic initiation. Iron ABC uptake systems, for example, are important effectors of virulence. There are two types of caspases&colon; initiators and effectors. Chk1 interacts with many downstream effectors to induce cell cycle arrest. Also plant resistance protein recognize bacterial effectors and programs resistance through ETI responses. The T3SS-1 enables the injection of bacterial effectors within the host cytosol. The RhoA pathway promotes assembly of the actin-myosin ring by two main effectors. These include structural proteins of the NC, effectors and chaperones. Other artificial restriction enzymes are based on the DNA binding domain of TAL effectors.