SUMMARY: Plants have evolved a sophisticated immune system to defend against invasion by pathogens. In response, pathogens deploy copious effectors to evade the immune responses. However, the molecular mechanisms used by pathogen effectors to suppress plant immunity remain unclear. Herein, we report that an effector secreted by Ralstonia solanacearum, RipAK, modulates the transcriptional activity of the ethylene‐responsive factor ERF098 to suppress immunity and dehydration tolerance, which causes bacterial wilt in pepper (Capsicum annuum L.) plants. Silencing ERF098 enhances the resistance of pepper plants to R. solanacearum infection not only by inhibiting the host colonization of R. solanacearum but also by increasing the immunity and tolerance of pepper plants to dehydration and including the closure of stomata to reduce the loss of water in an abscisic acid signal‐dependent manner. In contrast, the ectopic expression of ERF098 in Nicotiana benthamiana enhances wilt disease. We also show that RipAK targets and inhibits the ERF098 homodimerization to repress the expression of salicylic acid‐dependent PR1 and dehydration tolerance‐related OSR1 and OSM1 by cis‐elements in their promoters. Taken together, our study reveals a regulatory mechanism used by the R. solanacearum effector RipAK to increase virulence by specifically inhibiting the homodimerization of ERF098 and reprogramming the transcription of PR1, OSR1, and OSM1 to boost susceptibility and dehydration sensitivity. Thus, our study sheds light on a previously unidentified strategy by which a pathogen simultaneously suppresses plant immunity and tolerance to dehydration by secreting an effector to interfere with the activity of a transcription factor and manipulate plant transcriptional programs. Significance Statement: Bacterial wilt blocks the vascular system of Ralstonia solanacearum. The resistance of plants to bacterial wilt has been hypothesized to be related not only to an immune response but also to their tolerance to dehydration. However, how R. solanacearum simultaneously suppresses plant immunity and dehydration tolerance of plants to facilitate infection remains unclear. We provide evidence that the R. solanacearum effector RipAK increases virulence during infection by interacting with and specifically inhibiting the homodimerization of ERF098 and reprogramming the transcription of immune‐associated PR1, dehydration‐related OSR1 and OSM1 to be directly regulated by ERF098 to boost susceptibility and sensitivity to dehydration. [ABSTRACT FROM AUTHOR]