This process is primarily mediated by the binding of BC-derived CSCL1-3 and CSCL8 to the CSCR2 receptor, consequently activating the extracellular regulated protein kinases (ERK)1/2 pathway and the transcription factors NF-κB and Stat3 in a paracrine fashion, leading to the initiation of LIF expression, which in turn upregulates CXCLs [66]. Here, LIF is linked to breast cancer.