This review aims to: (1) explore the link between metabolic dysregulation and immune dysfunction in FS, (2) examine the role of JAK-STAT signaling in chronic inflammation and fibrosis, (3) compare JAK-STAT signaling with other fibrotic pathways such as TGF-β, and (4) propose novel therapeutic strategies targeting metabolic–immune interactions in FS. This evidence concerns the gene TGFB1 and Feingold syndrome.