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Stripe rust, caused by <i>Puccinia striiformis</i> f. sp. <i>tritici</i> (<i>Pst</i>), stands out as one of the most devastating epidemics impacting wheat production worldwide. Resistant wheat varieties had swiftly been overcome due to the emergence of new virulent <i>Pst</i> strains. Effectors secreted by <i>Pst</i> interfere with plant immunity, and verification of their biological function is extremely important for controlling wheat stripe rust. In this study, we identified an effector, Pst-18220, from <i>Puccinia striiformis</i> f. sp. <i>tritici</i> (<i>Pst</i>), which was induced during the early infection stage of <i>Pst</i>. Silencing the expression of Pst-18220 through virus-mediated host-induced gene silencing (HIGS) resulted in a decreased number of rust pustules. In <i>Nicotiana benthamiana</i>, it significantly suppressed cell death induced by <i>Pseudomonas syringae</i> pv. <i>tomato</i> (<i>Pto</i>) DC3000. In Arabidopsis, plants with stable overexpression of Pst-18220 showed increased susceptibility to <i>Pto</i> DC3000, accompanied by a decrease in the expression level of pattern-triggered immunity (PTI)/effector-triggered immunity (ETI)-related genes, namely, AtPCRK1, AtPCRK2, and AtBIK1. These results emphasize the significant role of the <i>Pst</i> candidate effector, <i>Pst</i>-18220, in rust pathogenicity and the suppression of plant defense mechanisms. This broadens our understanding of effectors without any known motif.