SLC11A1 and leukemia: Studying leukemia cells representing committed myeloid progenitors with bi-potential differentiation capacity not only enables longitudinal study of the control of gene expression but to also address differences in locus activation, which may result from genetic and/or epigenetic variations such as those observed at SLC11A1 locus between HL-60 and NB4 cells or K-562 and CMK cells, and which in turn may inform on (epi)genetic processes relating to leukemogenesis.