Nevertheless, the studies establishing the TNIP1-SSc genetic association and/or the reduced TNIP1 expression levels in SSc samples [17, 18, 127, 142] are consistent with and supportive of TNIP1 as a key suppressor of pathways driving a fibrotic signaling whether intrinsic to the fibroblast or in a paracrine fashion where TNIP1 deficiency or defective function in associated epithelial cell (e.g., skin keratinocytes) could make these otherwise protective cells a source of fibroblast-activating cytokines. Here, TNIP1 is linked to systemic sclerosis.