In vitro studies using GPR35-deficient (Gpr35-/-) mice in Apcmin and azoxymethane/dextran sodium sulfate (AOM/DSS) models have demonstrated significant reductions in tumor burden, likely due to disrupted NKA-Src signaling and downstream effectors such as ERK1/2 and Akt (26). The gene discussed is AKT1; the disease is neoplasm.