In a mouse colorectal cancer model with CSCs marked with diphtheria toxin receptor (DTR) under control of the Lgr5 promoter, addition of diphtheria toxin ceased tumor growth as a result of ablation of Lgr5+ CSCs [262,263]; diphtheria toxin removal reproduced Lgr5+ CSCs and resulted in tumor regrowth [263]. Here, LGR5 is linked to neoplasm.