One study showed that overexpression of DCAF4L2, a paralog of DCAF4, could support (epithelial-)mesenchymal transition in colorectal cancer cells through activation of the NF-κB pathway [37], and genetic variations in DCAF4 have been previously associated with leukocyte telomere length, keloid formation and lung cancer risk [38,39,40]. The gene discussed is NFKB1; the disease is lung cancer.