The mechanisms of the DRS pathogenesis are not clearly defined, but it is known that this comorbidity can trigger the activation of monocytes and T cells combined with the overproduction of cytokines, such as interleukin IL-6, interferon γ [20,21], C-reactive protein (CRP), tumor necrosis factor (TNF-α), and other pro-inflammatory cytokines [5,8]. This evidence concerns the gene CRP and Duane retraction syndrome.