For instance, on the one hand, evidence suggested EGCG prevented a pro-inflammatory and tumor-associated adipocyte-like phenotype (with upregulated CCL2, CCL5, CXCL8, IL-1β, IL-6, COX2, HIF-1α, and VEGF) induced by TNBC secretome in adipose-derived MSCs, primarily through the inhibitory effects of EGCG on Smad2 and NF-κB signaling pathways (171). Here, NFKB1 is linked to neoplasm.