Duowei found that APOBEC3B increased transcriptional expression through the non-classical NF-κB signal pathway, while the increased expression of APOBEC3B significantly increased CCL2 chemokine, thus recruiting myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs) to participate in the development of HCC56. Here, NFKB1 is linked to neoplasm.