Given the lack of response to antihistamines, steroids, mycophenolate (suppressor of T-lymphocytic and primary antibody responses to antigens), Icatibant (selective, bradykinin B2 receptor antagonist), and fresh frozen plasma (replacement of defective C1 esterase inhibitor), it is likely that the acquired angioedema and urticaria-like lesions occurred without mastocyte degranulation and systemic histamine release, activation of the complement cascade, or excessive endogenous bradykinin production, suggesting local release of vasoactive molecules by the T cells infiltrating the skin. This evidence concerns the gene C1S and angioedema.