In our analysis of fibroblasts, FB1 was characterised as a pro-inflammatory or immune-interacting subtype by APOE, CYGB, C7, and IFGBP7 and this subset showed higher levels of CCL19 and PLA2G2A in scleroderma compared to the control (Figure 4) [7]. The gene discussed is PLA2G2A; the disease is scleroderma.