Two different hypotheses may be considered to explain the change in IL-6 production during the immune response to viral infection: (i) the increased ability of some viral strains to overcome the immune response using a variety of evasion strategies (Beachboard and Horner, 2016), and consequently up-regulate the production of IL-6 as a result of increased viral loads, and (ii) polymorphisms in the IL-6 gene promoter stimulating overexpression of IL-6 during the immune response, a fact that has been shown to correlate with HBV progression (Lan et al., 2015). The gene discussed is IL6; the disease is viral infectious disease.