Most skeletal bones are formed by endochondral ossification, during which osteoblasts replace a cartilage scaffold laid down by chrondrocytes with bone. Exactly how the proliferation and differentiation of chrondrocytes and osteoblasts is controlled during ossification is not known. On p. 4587, Peter Angel and co-workers report that JunB, a member of the AP-1 transcription factor family, regulates the proliferation and function of these cell types during endochondral ossification in mice. The JunB knockout is embryonic lethal; so the researchers developed two junB-/- Ubi-junB mouse lines, in which expression of JunB is controlled by the human ubiquitin C promoter. This rescued the embryonic lethal phenotype but resulted in reduced JunB expression in several adult tissues, including bone. Longitudinal bones were shorter in these mice than in wild-type mice and the expression of cyclin A, cyclin D1 and p16INK4a - key cell-cycle regulators - was deregulated in chrondrocytes and osteoblasts. Studies on conditional knockout mice, suggest Angel and colleagues, should help to determine the exact role of JunB in the osteoblastic lineage.