GSEA analysis found that, in the group with high expression of TNC in keloids, the enrichment pathways included skin development, fibroblast, cancer progression, neutrophil at skin wound, and uterine fibroid (Figure 9A); In the low TNC expression group, the enriched pathways included YBX1 targets, ES-1, proliferation, transformed by RhoA, and defetive CFTR cause cystic fibrosis (Figure 9B). The gene discussed is CFTR; the disease is keloid.