IL-10 exerts important anti-inflammatory effects by suppressing the immune response, acting as a negative regulator of the local cytokine microenvironment, and limiting antigen presentation.[31] The lack of IL-10 enhances T-cell activation and differentiation, resulting in a strong inflammatory reaction to infection.[32] TNF-α, a potent pro-inflammatory cytokine produced by macrophages and monocytes, has paradoxical anti-inflammatory properties.[33–36] In this study, significantly lower IL-10 and TNF-α levels were observed in the ROP group than in the non-ROP group. This evidence concerns the gene IL10 and infection.