However, when compared with the mock-infected counterpart, RA-treated HL60-siAgo2 cells showed a strong dose-dependent induction of two RA target genes related to granulocytic differentiation, such as the retinoic-acid-receptor beta (RARβ) and the transglutaminase type-II (TGase-II) (Figure 3a).37 This observation and the fact that Ago2 expression decreases during RA-induced differentiation (Figures 1b–d) led us to hypothesize a role for Ago2 silencing in granulocyte differentiation of myeloid progenitors and APL cells. The gene discussed is AGO2; the disease is acute promyelocytic leukemia.