It is currently unknown whether EPOR in cancer cells exists as a homodimer or as a heterodimer [with the common-β receptor subunit (CD131)] with a much lower EPO affinity (50, 51), whether EPOR activation is ligand-independent (52), or whether endogenously produced EPO, either by the kidney or by the tumor itself (2, 10, 53), is sufficient to fully activate EPOR in A549 tumors. This evidence concerns the gene EPO and cancer.