Interestingly, we observed increased activation of anti-tumor immune-related pathways (STAT4/JAK2 and Type-I IFN signaling) and inhibition of BCSC regulators (β-CATENIN and NF-κB pathways) in HGFL-RON signaling-deficient BCSCs compared to controls. The gene discussed is NFKB1; the disease is neoplasm.