Given the established role of p38 in skeletal development and its mediation of SPC senescence in cranial suture homeostasis maintenance in Crouzon syndrome mice, we further analyzed RNA-seq data from craniosynostosis tissues and cells in public databases (human and murine) to investigate whether p38 MAPK-mediated cellular senescence is universally implicated in craniosynostosis pathogenesis. Here, MAPK1 is linked to Crouzon syndrome.