Specifically the stimulation by interleukin-1 and TNF-α was shown to increase plasma levels of PTX-3. This effect was shown in various cells and inflammatory steps, such as during the initial phase of inflammation by recognizing pathogens and activation of the complement pathway, thus allowing an approach to explain the early elevated PTX-3 plasma levels in patients with infection [11, 12, 23]. The gene discussed is PTX3; the disease is infection.