In their natural settings, plants are constantly exposed to hostile conditions including biotic and abiotic stresses. Plants interact with a plethora of microorganisms leading to bene-ficial or deleterious interaction, unleashing plant defense mechanisms, including constitutive and induced resistance. Constitutive resistance is also referred as the nonhost-resistant mech-anisms to sense and to resist the attack from a great proportion of pathogens. This first defense mechanism includes a structural layer and chemical constitutive. The structural layer is part of plant physical barriers, including the cuticle, trichomes, and waxes. The constituent chemicals are toxic compounds secreted by plant cells. Once microorganisms overcome the plant physical barriers, the plant defense systems are triggered, with the subsequent attempt of microorganism to suppress plant immunity to succeed in diseases or to set up a beneficial relationship (Yang and Huang, 2014). In addition to constitutive defense, plants have evolved additional immune layers, including the Microbial or Pathogen-Associated Molecular Pat-terns (MAMPs or PAMPs, respectively) trigger immunity (PTI). After recognition of MAMPs or PAMPs through cell surfaceelocalized pattern recognition receptors, plants synthesize secondary metabolites (SMs) with antimicrobial activity such as phytoalexins, accumulate hy-drolytic enzymes, and reinforce the plant cell wall by deposition of callose (Hématy et al., 2009). It is well-known that PAMPs and MAMPs induce the systemic acquired resistance (SAR) through the phytohormone salicylic acid (SA), which is highly accumulated at the infection site, and subsequently the signal spreads to distant parts of the original site of infec-tion. The SAR signaling induction parallels well with the expression of a set of genes coding for proteins related to pathogenicity (PR) (Pieterse et al., 1996). SAR signaling is effective against biotrophic and hemibiotrophic microorganisms such as the bacterial pathogen Pseu-domonas syringae pv. tomato (PstDC3000) and the fungal pathogen Colletotrichum spp. (Hammond-Kosask and Jones, 1997). Moreover, beneficial microorganisms boost the induced systemic resistance, which is dependent on the synthesis of the phytohormones jasmonic acid and ethylene (JA/ET). In this case, LOX-2 and PDF1.2 genes, which code for the lipoxygenase-2 and a plant defensin, respectively, are induced in Arabidopsis (Jakob et al., 2007). The JA/ET signaling is effective against the necrotrophic pathogens such as the fungus Botrytis cinerea. Additionally, SA and JA/ET pathways can affect each other, either negatively or synergistically. The cross-talk between SA and JA/ET pathways provides potential for the activation of multiples resistance mechanisms, driving plants to prioritize a particular defense pathway against the attacker (Pieterse and Van Loon, 2004). On the other hand, pathogens have evolved effector molecules to suppress the PTI and succeed in disease into the host. In response, plants have developed resistance proteins that recognize effectors to promote effector-triggered immunity (ETI) (Chisholm et al., 2006). During ETI, plants trigger the hy-persensitive response (HR), a form of programmed cell death at the site of infection to delimit the pathogen and prevent its spreading to other parts of the plant (Nomura et al., 2005). Furthermore, after the plant is attacked by a pathogen or a beneficial microbe colonizes the root, plants show strong defense abilities against further pathogen infections. This response is the so-called “priming” (a hypersensitized state), which is a faster and more effi-cient response, compared with plants that were not attacked by pathogens or colonized by beneficial microorganisms (Conrath et al., 2006).