Although S100A8/A9 has pro-tumor effects, evidence suggests that high concentrations of S100A8/A9 can paradoxically inhibit tumor growth.220 For instance, overexpression of S100A9 can trigger apoptosis in NB4 cells (acute promyelocytic leukemia cells).220 Moreover, S100A8/A9 participates in complex networks of signaling pathways, and mechanistic studies are largely confined to theoretical research. The gene discussed is IGKV1D-22; the disease is neoplasm.