The capacity of apigenin to block CCL2 is important because this single event is not only in control of infiltrating/migratory activity of CAFs, TAMS, TANS, and MSCs into the tumor environment but enables its perpetual ongoing accelerated release of CCL2, CXCL8, CCL5, mediated by through NF-kB signaling [24]. Here, CCL5 is linked to neoplasm.