Subsequently, we found that activation of NF-κB in the GATA6-overexpressing human CRC clones was dependent mainly on the EGFR/AKT pathway (Figure 5) which could be attributed to the dramatic increases of both the total and surface levels of CD44 in these clones [43] because this CRCSC marker was well documented as a co-receptor in the EGFR signaling pathway [68,69,70]. This evidence concerns the gene NFKB1 and colorectal carcinoma.