As this mutation resulted in a Dicer-dependent translational repression of a reporter gene, the consequence could be a translational repression of TNFAIP2, previously described as a target of PML-RARA or PZLF-RARA fusion genes and highly expressed in hematopoietic cells. TNFAIP2 mutation was predicted to generate imperfect binding sites for miR-223 and miR-181b, but the experiments conducted on AML cell lines did not confirm contribution of miR-223 and miR-181b and any other known miRNA to the translational repression of mutant TNFAIP2 3′-UTR. The gene discussed is RARA; the disease is acute myeloid leukemia.