Combining the fact that IGF1R and IR can form a hybrid disulfide-linked heterodimer and that dual knockdown of IGF1R + IR more effectively reduced collagen and fibronectin than IGF1R or IR alone, the hybrid receptor most likely represents a significant receptor species contributing to fibrosis mediated by IGF-II, and thus also represents a likely therapeutic target for the treatment of SSc. This evidence concerns the gene FN1 and systemic sclerosis.