Notably, B cells play a pivotal role in the pathogenesis of SSc by producing cytokines such as IL-6 and TGF-β (25, 26), engaging in self-activation with T cells (27), stimulating fibroblasts (28), and contributing to endothelial cell activation and injury (29, 30), among other pathways, which ultimately lead to the inflammatory and fibrotic phenotypic manifestations of SSc. Here, TGFB1 is linked to systemic sclerosis.