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Based on a screen in our lab, aimed at identifying mutants with an impaired endodermal diffusion barrier in their roots, we identified a group of mutants that we termed SCHENGEN (SGN) mutants. These were idenitiifed as an LRR receptor-like kinase SGN3 (also called GSO1), a non-transmembrane kinase (SGN1), the NADPH oxidase RBOHF (SGN4), as well as TPST (SGN2) an enzyme responsible for sulfating a number of peptide ligands. I will report on our research in recent years, allowing us to place all SGN mutants into a novel signaling pathway. This pathway appears to have evolved for surveillance of diffusion barrier integrity and assists the differentiating endodermis in formation of a continuous and tightly sealed Casparian strip network. Intriguing variations of this pathway appear to be at play in the control of embryonic cuticle formation. The SCHENGEN pathway is unusual because it detects defects in subcellular structures by making use of the restricted subcellular localization of its signaling components. At the same time, the basic pathway components identified bear striking homologies to plant immune receptor pathways, prompting speculations that the pathway could represent a neo-functionalisation of ancient stress response pathways.