Given that autophagy has been implicated in the granulocytic differentiation of APL cells and that the degradation of the PML/RARα oncoprotein by ATRA is autophagy-dependent [13], we investigated the protein levels of LC3B-II, p62 and PML/RARα in NEAT1-silenced NB4 cells, both before and after ATRA treatment. The gene discussed is PML; the disease is acute promyelocytic leukemia.