Because recent in vivo studies at the William Harvey Institute [17], with other corroborative markers, show quite clearly that high-dose OHCbl, and particularly GSCbl, promote iNOS mRNA in the early stages of LPS-induced inflammation, and because mice given high-dose Cbl to treat LPS-induced sepsis show remarkable survival [55], it is possible that Cbl first promotes iNOS NO production and later, in the resolution phase of inflammation, inhibits it, perhaps over and above iNOS inhibition by NO itself. Here, NOS2 is linked to Sepsis.