Phosphorylated JAK2 is involved in the phosphorylation of tyrosine residues in EPOR cytoplasm; these residues can bind to the SH2 domain of STAT5; when brain trauma occurs, STAT5 activity can be inhibited by negative feedback factors such as SOCS-3 activated by proinflammatory cytokines, thereby preventing EPO’s intracellular signal transduction and weakening EPO’s neuroprotective effect (82); this pathway can be blocked by JAK2 inhibitors (83). Here, EPO is linked to brain injury.