We suggested that the suppression of PGE2 production by cold medicines might contribute to the pathogenesis and onset of CM-SJS/TEN with SOC (1, 4, 6, 8, 11, 22) because PGE2 acts on EP3 and negatively regulates mucocutaneous inflammation (24–26). The gene discussed is PTGER3; the disease is toxic epidermal necrolysis.