To validate the role of PRLR in clonogenicity, the U-937 AML cells, that express the highest level of this receptor in the surface (Fig. 1E), were edited with a CRIPR/Cas9-based lentiviral system to knock out PRLR up to 2.57-fold (Fig. 2H). The gene discussed is PRLR; the disease is acute myeloid leukemia.