In FD, the combination of IL-17A and TGFβ signaling in fibroblasts can potentiate more robust ECM gene expression than either cytokine alone.329 Add outside-in sensing of the stiff fibrotic matrix and hypoxia on top of the synergy between IL-17A and TGFβ, and this combination is likely part of what drives fibroblast to deposit pathogenic ECM in FD. Here, IL17A is linked to Fabry disease.