Recently, a constitutive ligand-independent pro-cancer function of GPR35 was reported, demonstrating that GPR35 interacted with Na+/K+-ATPase inducing colorectal cancer (CRC) cell proliferation and glycolysis (Schneditz et al., 2019), also driving macrophages to promote angiogenesis in the tumor microenvironment (Pagano et al., 2021). The gene discussed is GPR35; the disease is colorectal carcinoma.