The increased level of NFκB was accompanied by a decrease in the level of the NFκB inhibitor, i.e., IκBα, which, in turn, could have contributed to the observed increase in the level of the product of NFκB transcriptional activity, i.e., TNFα, both in the group of patients who survived and in those who did not survive the infection (Figure 3). Here, NFKB1 is linked to infection.