Although the PML-RARα translocation appears to enhance the sensitivity of APL to atRA and several intrinsic mechanisms of atRA resistance have been identified, including overexpression of Tal1, expression of PRAME as well as epigenetic silencing or mutation of RARα [4–7], the majority of non-APL AMLs and even other cancers remain sensitive to atRA in vitro[7–12]. The gene discussed is RARA; the disease is acute promyelocytic leukemia.