In a study focused on LPS-induced septic lung injury in mice, it was noted that the silencing of TREM2 could precipitate the downregulation of SHP1 and an increase in the phosphorylation of STAT3; conversely, the overexpression of TREM2 could mitigate oxidative stress and ferroptosis via the SHP1/STAT3 pathway, thus significantly alleviating sepsis-induced acute lung injury (62). This evidence concerns the gene TREM2 and Sepsis.