A proposed model for the mechanism of action underlying low expression of the CYP26 cytochrome as a potent cause of relapse. The hypothesis that the growth of APL-resistant blasts is provoked by an increased exposure to active retinoids is based on the observation that, by studying the kinetics of differentiation, cytochromes involved in ATRA metabolism are differently activated between low- (A) and high-sensitive (B) APL cells.