CD47 and fibrosis: Promoter accessibility of all 3 genes was increased in scleroderma fibroblasts, and JUN knockout led to decreased promoter accessibilities of CD47, PDL1, and IL6. Finally, ATAC-Seq demonstrated distinct promoter accessibility clustering before and after JUN knockout in scleroderma fibroblasts and increased promoter accessibilities of several fibrosis-associated genes (Figure 2, C and D).