Studies have indicated that, in dermatitis, cytoplasmic HMGB1 activates the PI3K/AKT/NF-κB and ERK/NF-κB signalling pathways, which contributes to increased expression of HMGB1 and its receptors, such as RAGE and TLR4, as well as the subsequent production of proinflammatory cytokines, such as TNF-α and IL-6 (62). Here, NFKB1 is linked to skin disorder.