ESR1 and neoplasm: Additionally, Benhadjeba et al., through in vitro experiments on EOC cell lines, proved a feed-forward mechanism between ERα and the CXCR7/CXCL11 chemokines axis, which activates Erk1/2 and phosphorylates ERα at Ser-118, leading to a more aggressive pro-metastatic tumor phenotype [41].