In case of bacterial infection, specific proinflammatory cytokines such as lipopolysaccharide (LPS), interleukin-1beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) as well as microbial toxins (endotoxins) stimulate CALC-I gene expression, and then the release of PCT is increased from diverse parenchymal tissues previously described [27]. Here, CALCA is linked to bacterial infectious disease.