Ca2+-dependent eNOS and nNOS produce NO continuously in short puffs and low amounts, with some modest up-regulation in inflammatory immune response, and up-regulation or depression in pathologies of unresolved inflammation, such as tumour growth or sepsis: Ca2+ independent iNOS, which is dependent for its expression on the transcription factors, NFκB, STAT-1, AP-1 and IRF-1 [141,158], can yield a 700–1000-fold greater increase in NO in a very short space of time. Here, NOS1 is linked to Sepsis.