Consistently, the expression levels of FAK, PIK3CA and CD274 were significantly downregulated after KPNA4 knockdown, whereas AKT1 expression had nothing to do with KPNA4. Overall, our results suggested that KPNA4 may promote FAK signaling and PD-L1 expression in PDAC cells, which could be responsible for the KPNA4-dependent malignant behaviors of cancer cells and immunosuppressive TME in PDAC patients. The gene discussed is AKT1; the disease is cancer.