KPNB1 and dentin dysplasia: Specifically, ALOX5 might activate the inflammatory response system through histone acetylation mechanisms, thereby triggering DD; JDP2 could regulate ROS levels to influence histone acetylation, playing a pivotal role in controlling depression-related gene expression and offering guidance for individualized therapy; while KPNB1 may serve as a crucial mediator in neurotransmission and intracellular signaling pathways, facilitating assessment of disease progression and therapeutic efficacy in DD.