The increase in ROS cause Th1 and Th17 cells and keratinocytes to activate the MAPK, NF-κB and JAK-STAT pathways [130, 131], thereby forming a self-amplification cycle that ultimately leads to excessive keratinocyte proliferation, vascular proliferation and inflammatory infiltration, which is also characteristic of psoriasis [132]. Here, NFKB1 is linked to psoriasis.