As phosphatase and tensin homolog (PTEN) is one of the primary targets of PML/RARA in APL (Noguera et al., 2016), and loss of PTEN protein plays a critical role in determining the disease severity in myeloid malignancies (Liu et al., 2016), up-regulation of non-mutated PTEN by PGZ (Patel et al., 2001) could be an additional molecular mechanism explaining the combined activity of ATRA/AZA/PGZ. The gene discussed is RARA; the disease is acute promyelocytic leukemia.