When KPNB1 is knocked down, it not only disrupts the essential odontoblastic differentiation potential of DPSCs but also leads to the accumulation of ATF4 in the cytoplasm, similar to the effect reported in glioma cells when KPNB1 is knocked down, causing endoplasmic reticulum (ER) stress and the upregulation of ATF4, an ER stress response molecule [69]. This evidence concerns the gene ATF4 and central nervous system cancer.