WNT3A and craniosynostosis: Wnt signaling has previously been shown to be functionally related to osteogenic differentiation, where Wnt family member 3A (WNT3A), which regulates β‐catenin, is essential for the development of the skull.[31] Notably, circPROSC exhibited a positive correlation with WNT3A and β‐catenin, which were highly expressed in the skulls of craniosynostosis patients, accompanied by increased nuclear β‐catenin levels and elevated expression of the downstream targets LEF1 and TCF7 (Figure 3C–E; Figure S8, Supporting Information).