Since signaling machineries for two modes of plant‐induced immunity, pattern‐triggered immunity (PTI) and effector‐triggered immunity (ETI), extensively overlap, PTI and ETI signaling likely interact. In an Arabidopsis quadruple mutant, in which four major sectors of the signaling network, jasmonate, ethylene, PAD4, and salicylate, are disabled, the hypersensitive response (HR) typical of ETI is abolished when the Pseudomonas syringae effector AvrRpt2 is bacterially delivered but is intact when AvrRpt2 is directly expressed in planta. These observations led us to discovery of a network‐buffered signaling mechanism that mediates HR signaling and is strongly inhibited by PTI signaling. We named this mechanism the ETI‐Mediating and PTI‐Inhibited Sector (EMPIS). The signaling kinetics of EMPIS explain apparently different plant genetic requirements for ETI triggered by different effectors without postulating different signaling machineries. The properties of EMPIS suggest that information about efficacy of the early immune response is fed back to the immune signaling network, modulating its activity and limiting the fitness cost of unnecessary immune responses. Synopsis A systems‐based analysis reveals crosstalk between pattern‐ and effector‐triggered plant immunity that enables modification of immune responses based on efficacy of early immune responses. The plant immune signaling network contains a signaling sector that mediates effector‐triggered immunity (ETI) and is inhibited by pattern‐triggered immunity (PTI). This signaling mechanism is named ETI‐mediating and PTI‐inhibited sector, or EMPIS. EMPIS mediates ETI in a compensatory manner with other signaling sectors. Differences in the timing of ETI and PTI signals reaching EMPIS determine qualitative differences in EMPIS requirements for ETI response triggered by different pathogen effectors. A systems‐based analysis reveals crosstalk between pattern‐ and effector‐triggered plant immunity that enables modification of immune responses based on efficacy of early immune responses.