Consistent with our prediction, treating primary EGCs with IL-1β markedly activated the CRC EGC phenotype, with induction of Lcn2 and Timp1, and immunomodulatory factors Ccl2 and Il6, both at RNA and protein level, highlighting a specific molecular EGC response independent of embryonic or adult neurosphere origin (Fig. 4d, e, Supplementary Fig. 5c, d and Supplementary Data 2). The gene discussed is CCL2; the disease is colorectal carcinoma.