NFKB1 and Sepsis: In HK-2 cells (a classical model of sepsis-induced renal injury in vitro), PTPN2 reduced LPS-induced inflammatory cytokine release and cell death via modulating p38 MAPK/NF-κB signaling, which alleviated renal cell damage by playing a nephron-protective role in sepsis-induced renal injury (Figure 2) [40].