Finally, the facts that ITPR1 is expressed in the sensory DRG, the trigeminal ganglia and the substantia gelatinosa [3], in which C fibre axons synapse with neurons of the pain-transmitting lateral spinothalamic tract and damage to which can cause pain and hyperalgesia, and that ITPR1 dysregulation has been implicated in hyperalgesia and allodynia in animal studies [5], along with the presence of a severe pain syndrome in our patient, provide a preliminary rationale for seeking a potential role of ITPR1-related autoimmunity also in patients with pain syndromes of unknown aetiology. The gene discussed is ITPR1; the disease is Autoimmunity.