Clinical and experimental studies have confirmed that when oral ulcers occur, abnormally activated macrophages in the oral mucosa secrete a large number of proinflammatory factors, and the activated NF-κB inhibitory protein (IκB) kinase complex promotes NF-κB translocation to the nucleus, indirectly initiating the expression of genes such as the proinflammatory factors TNF-α and IL-1β, and inhibiting the expression of anti-inflammatory factors. Here, NFKB1 is linked to Oral ulcer.