Psoriasis is a skin disorder characterized by involvement of the skin by red, scaly patches (plaques). It is a genetic skin condition due to a defective gene on the 17th chromosome. Although this disease is present at birth, psoriasis usually develops only after some form of injury to the skin (trauma, infection, allergic reaction). Non-skin infections (e.g. urinary tract infections) may also precipitate psoriasis. These cause release of phosphorylase kinase (PhK), an enzyme responsible for converting glycogen into ATP, the form of energy required for wound healing processes. PhK activity increases after injury and decreases after healing. Patients with the psoriatic gene appear to be unable to reduce the increased PhK activity caused by injury. This results in persistence of the healing processes including rapid formation of skin barrier (stratum corneum) cells every 4 days (defective barrier) in psoriatic skin, compared to every 60 days (good barrier) in normal skin). The psoriatic skin, when it is formed very quickly, is defective in providing the barrier function necessary to prevent infection or block chemicals from entering the skin. It is this genetic inability to correct the poor barrier (resembling a jellyfish) that causes persistence of psoriasis.