Psoriasis is widely regarded as a multifactorial disorder caused by the interaction between inherited susceptibility alleles and environmental factors. The known genetic susceptibility alleles highlight that both adaptive and innate immunity pathways are involved in the pathogenesis of psoriasis.1 In people who are genetically susceptible, the actual onset of psoriasis canbe triggered by stimuli such as mild mechanical trauma, streptococcal infection of the upper respiratory tract, stress, sunburn, or some systemic medications (eg, β blockers, lithium, antimalarials).4 These stimuli provoke the production of interleukin (IL)-23, which induces several cytokines (including IL-17) that, in turn, directly or by secondary mediators, alter the function of keratinocytes and other skin tissue cells