Because these phenotypes seemed to be similar to those of laminopathy-based premature aging, we investigated the state of the lamin A. We identified an accumulation of abnormal lamin A (prelamin A), accompanied by a reduction in the Zmpste24 expression in the GMF-TG mice, suggesting that accelerated aging phenotypes in the GMF-TG mice might be associated with this laminopathy, caused by prelamin A accumulation. Here, GMFB is linked to laminopathy.