Using a mouse colon carcinoma model, Yoshii et al. further demonstrated that [64Cu][Cu(ATSM)] preferentially accumulated in regions with high CD133+ expression, a common marker of CSC, which is believed to be the origin of self-renewal and differentiation ability of many tumor types and a major contributor to therapeutic resistance and metastasis [20, 52–56]. The gene discussed is PROM1; the disease is colon carcinoma.