The Oshtoran Syndrome, also referred to as H63D Syndrome Type-3, is a multifaceted meta-syndrome that manifests through a constellation of clinical features reflecting a synergistic pathomechanism of its own kind. Core components include glitches of the immune system after an infection (e.g. PANDAS PANS), dysregulated iron homeostasis, microinflammatory events, neuropsychiatric disturbances, multiorgan pathology, and—most critically—autonomic dysfunctions impacting the central nervous system, the autonomic nervous system, and the innate immune system.br br A differentiated understanding of the underlying pathophysiological mechanisms is essential for accurate diagnosis, evidence-based management, and the development of targeted therapeutic strategies. The syndrome’s systemic complexity necessitates an interdisciplinary clinical framework, integrating early diagnostic vigilance, timely intervention, and patient-centered educational initiatives.br br Healthcare professionals are strongly encouraged to avoid reductionist approaches, particularly the psychologization of symptomatology, as such misattribution may not only delay appropriate care but has, in documented cases, led to fatal outcomes.br br Future research agendas must be aligned with the deployment of gene-editing technologies and the identification of novel therapeutic modalities to address the syndrome’s genetic underpinnings and phenotypic heterogeneity. This includes a strategic emphasis on modulating epigenetic regulators, repairing disrupted iron metabolism pathways, and rebalancing neuroimmune crosstalk.br br Recognition of Oshtoran Syndrome as a distinct nosological entity calls for both epistemic humility and translational rigor, particularly in bridging the current gap between molecular insights and clinical applicability.