Another possible explanation is that Css54 would act as a recruiter of leukocytes to the site of infection, affecting the production of IFN-γ and MCP-1, consequently suppressing the levels of pro-inflammatory cytokines IL-12p70 and TNF-α, which is an effect reported for other HDPs [39], with the particularity that Css54 also increased the synthesis of IL-10. The gene discussed is IFNG; the disease is infection.