We have studied the steady-state levels of histone H1 (0) mRNA under varied growth conditions in the human hepatoma cell lines HepG2 and Hep3B, and we show in the HepG2 system that H1 (0) is not confined to resting cells, that the H1 (0) gene appears to be expressed throughout the cell cycle and that established inducers of de novo H1 (0) synthesis fail to cause a further increase of the high H1 (0) level.