Our research group reported that while SALL4 and its interacting epigenetic factor LSD1 inhibited ATRA-induced granulocytic differentiation, co-inhibition of SALL4, LSD1, plus ATRA treatment severely disrupted ATRA-resistant AML cell growth, and blocked HL60 AML xenograft tumors by ~91%, while the treated mice exhibit no signs of illness [62, 79]. The gene discussed is SALL4; the disease is acute myeloid leukemia.