Murine erythroleukemia cells provide a model for the study of erythropoietic differentiation uncoupled from the normal requirement for erythropoietin for cell proliferation. Evidence is presented which suggests that differentiation-inducing chemicals may have a number of cellular sites of action, including effects at the plasma membrane and on chromatin, but a common pathway may include a transient delay of the cell cycle in G1, alterations in chromatin structure, and the expression of a complex pattern of gene transcription responsible for the program of differentiation.