The pathomechanistic concepts proposed for the disease (7, 8) include i) blockage of the sweat gland duct and induction of symptoms by sweat leakage into the tissue (9); ii) IgE-mediated mast cell activation induced by sweat antigen(s) (10), supported by the fact that therapy with the anti-IgE antibody omalizumab can be beneficial in CholU patients (11–13); and iii) association with reduced sweating (hypohidrosis) or complete lack of sweating (anhidrosis) in at least some body areas (8, 14, 15). The gene discussed is IGHE; the disease is hypohidrosis.