Plant immune genes are traditionally classified as resistance genes, susceptibility genes, or positive/negative regulators of defense. However, this framework does not fully explain a subset of immune-associated genes that display paradoxical disease phenotypes, in which genetic disruption enhances resistance despite the normal involvement of these genes in defense-related processes. GSL5/PMR4 is a representative example. As a pathogen-induced callose synthase, GSL5 contributes to papillary callose deposition and structural defense. Paradoxically, loss of GSL5 confers resistance to powdery mildew through salicylic acid- and N-hydroxypipecolic acid-associated pathways, as well as broad-spectrum resistance to Plasmodiophora brassicae through jasmonic acid-dependent immunity. Here, we refer to such genes as dual-state immune regulators, whose functional presence and genetic disruption promote resistance through distinct immune states. Similar regulatory patterns have been reported in several immune-related processes, including MAPK signaling, calcium influx, membrane trafficking, and receptor-proximal immune signaling. Representative examples include the MEKK1–MKK1/MKK2–MPK4 module, CNGC2/CNGC4, EXO70B1 and BIK1. This review uses GSL5 as a central example to discuss paradoxical immune phenotypes and dual-state immune regulators in plants, focusing on their biological features, potential mechanisms, and implications for resistance breeding.