These observations implicate microbial dysbiosis as a driver of heightened MRGPRX2-dependent activation, linking epithelial barrier disruption to neuroimmune dysregulation and non-histaminergic itch.Notably, although disease-specific triggers—such as neuropeptide sensitization in PsO, microbial dysbiosis in AD, and hapten-induced pruritus in ACD—differ in etiology, these mechanisms converge on a shared MRGPRX2–neuroimmune axis. This evidence concerns the gene MRGPRX2 and granular corneal dystrophy type II.