reported that in sepsis, EGFR promotes CD4+ T cell apoptosis by facilitating glucose transporter 1 (Glut1) translocation to the cell surface via the TANK‐binding kinase 1 (TBK1)/Exo84/RalA pathway, and EGFR inhibitors effectively alleviated the decrease in total CD4+ T cells in septic mice[345] (Figure 5C). This evidence concerns the gene SLC2A1 and Sepsis.