This prompted us to ask whether GPR35 on LysM+ cells, which encompasses macrophages and neutrophils,33 might mediate a TME pathway that promotes tumour growth.17 18 We, therefore, generated Apcmin allele-carrying mice with LysM-specific Gpr35 deletion (Gpr35fl/fl;LysM-Cre;Apcmin/+, ‘Gpr35ΔMΦ;Apcmin’) and compared them to their Gpr35-sufficient controls (Gpr35fl/fl;Apcmin/+, ‘Gpr35fl/fl;Apcmin’) (figure 1E). The gene discussed is GPR35; the disease is neoplasm.