Interestingly, EXOSC5 knockdown inhibit phosphorylation of AKT and STAT3, while EXOSC5 overexpression contributed to the activation of AKT and STAT3 (Figure 5B), so these data demonstrated that AKT and STAT3 signaling pathways were involved in the progression of GC regulated by EXOSC5. The gene discussed is AKT1; the disease is gastric cancer.