Moreover, selective recruitment of regulatory B cells, which express on their surface the chemokine receptor CXCR3 (CXCR3), are implicated in bridging the pro-inflammatory IL-17 response and the polarization of tumorigenic macrophages (M2-type) within the tumor environment, suggesting that inhibiting the migration or function of CXCR3+ B cells could potentially attenuate HCC progression [139,140]. The gene discussed is IL17A; the disease is neoplasm.