Chronic inflammation is a hallmark of TIME in TNBC and is primarily driven by signaling cascades such as the nuclear factor kappa B (NF-κB) pathway and pro-inflammatory chemokines such as the chemokine (C-C motif) ligand 2 (CCL2), which recruit tumor-associated macrophages (TAMS) and other immune-suppressive cell types [16]. This evidence concerns the gene NFKB1 and neoplasm.