Three of these genes were linked to a cartilage formation/repair endotype, namely growth differentiation factor 5 (GDF5), fibroblast growth factor 18 (FGF18), and transforming growth factor-beta 1 (TGF-β1) [10], suggesting that cartilage formation, when impaired, may be associated with a higher level of OA structural disease progression due to repair attenuation. This evidence concerns the gene TGFB1 and glycogen storage disease VI.