Specifically, previous studies reported that IL-6 activated by NFκB could promote CAC progression via the NFκB/IL-6/Stat3 cascade; among them, NFκB is a significant regulator of the growth and survival of tumor-initiating IECs and following the release of IL-6 could induce the recruitment and subsequent phosphorylation of JAK2 and Stat3 [35]. This evidence concerns the gene NFKB1 and neoplasm.