Future studies should investigate whether OC disrupts this PAR-2/RAC1/β-catenin axis in IDH-mutant CHS models, leveraging its dual capacity to downregulate PAR-2 [150] and preserve repressive H3K27me3 epigenetic marks [132] to counteract CpG island hypermethylation at tumor suppressor loci such as CDKN2A. The gene discussed is CDKN2A; the disease is neoplasm.