The pathogenesis of psoriasis involves genetic predisposition, immune dysregulation—particularly T helper 17 (Th17) cell polarization and interleukin-23/interleukin-17 (IL-23/IL-17) axis activation—cytokine network imbalances, keratinocyte dysfunction, and cascades of inflammatory mediators [6,7,8,9,10,11,12,13]. This evidence concerns the gene IL37 and psoriasis.