In addition, we found that ITLN1 induced the KLF4 expression via inactivation of PI3K/AKT signaling, which was required for ITLN1-mediated up-regulation of NDRG2 in NB cells, suggesting the tumor suppressive roles of ITLN1/KLF4/NDRG2 axis in the tumorigenesis of NB. The gene discussed is NDRG2; the disease is neoplasm.