Cardiac fibrosis has a central role in AFD progression, driven by pro-inflammatory and pro-fibrotic cytokines through pathways such as TGF-β, NF-κB, MAPK/ERK (Mitogen-activated protein kinase/Extracellular signal-regulated kinase), and the renin-angiotensin system. This evidence concerns the gene TGFB1 and Nager acrofacial dysostosis.