In response to burns injury, immune cells, including monocytes, macrophages, and neutrophils, are activated within hours to recognize endogenous factors such as DAMPs, activate downstream NF-κB inflammation-related signaling pathways, and promote inflammatory mediators (IL1, IL6, IL8, IL18, and TNF) release, ultimately leading to the development of systemic inflammatory response syndrome (Singer et al., 2016). Here, NFKB1 is linked to systemic inflammatory response syndrome.