Therefore we hypothesized that the decreased expression of the miR-23a/27a/24-2 cluster in TAMs of breast cancer patients might be related to the tumor microenvironment or tumorigenic factors including the activation balance between NF-κB and STAT6 pathway, etc. Taken together, our data demonstrate that the miR-23a/27a/24-2 cluster is a potential therapeutic target due to its ability to regulate TAM phenotype switching, resulting in the remodeling of the TME. The gene discussed is NFKB1; the disease is neoplasm.