Consistently, treating mice with Wnt5a, the critical pro-angiogenic factor regulated by FOSL2, could partly rescue blood vessels and tumor growth of tumor burden mice injected with FOSL2-silenced CAFs (labeled CAF/shFOSL2 + rWnt5a) in comparison to their control tumors (labeled CAF/shFOSL2). The gene discussed is FOSL2; the disease is neoplasm.