The sustained high expression of TNF-α and IFN-γ may lead to delayed inflammation and the formation of chronic wounds, while the overexpression of IL-6 may promote the expression of chemokines, attracting macrophages to the infection site, thereby maintaining a chronic inflammatory state and delaying wound healing (Weigelt et al., 2009; Lee et al., 2019). The gene discussed is IL6; the disease is infection.