Since several studies have already demonstrated that CD44 could be both a co-regulator and a downstream target of EGFR signaling [55,56] plus EGFR-induced AKT could activate NF-κB in HCT-8 human CRC cells [57], we postulated that EGFR signaling might be more active in the stemness-high GATA6-overexpressing human CRC clones. The gene discussed is NFKB1; the disease is colorectal carcinoma.