The pathophysiology of psoriasis is related to complex interactions between various immune, cellular, and molecular factors, in addition to the genetic and protein expression of various inflammatory mediators, such as interleukins (IL)- 6, -17, -22, and -23, interferon-gamma (IFNγ), nuclear factor kappa B (Nf-κB), and tumor necrosis factor-alpha (TNF⍺), as described by Croxford et al. [6], Ha et al. [7], Lowes, Suarez-Farinas, and Krueger et al. [8], and Raphael et al. [9]. The gene discussed is IFNG; the disease is psoriasis.