During bacterial infections, plasmatic PCT levels increase because lipopolysaccharides (LPS) and the inflammatory cytokines specific to bacterial infection, such as interleukin-1 beta (IL-1β), IL-6 and tumor necrosis factor-alpha (TNF-α), stimulate the upregulation of the expression of the CALC-1 gene in multiple tissues, leading to a massive production of PCT from many tissues [12,14]. This evidence concerns the gene IL1B and bacterial infectious disease.