Chronic graft vs host disease (cGVHD) is a complication of allogenic (allo) haematopoietic stem cell transplant (Tx) which manifests fibrosis similar to scleroderma. Endothelial injury occurs in GVHD pathogenesis but its role in cGVHD fibrosis is not elucidated. In the normal and pathological settings, bipotent endovascular progenitors (EVPs) self-renew in blood vessels and proliferate into differentiated endothelial (D) cells to maintain endothelium or undergo endothelial to mesenchymal cells (EndMT) to trigger fibrosis through Sox9 expression. We hypothesise that EndMT promotes skin cGVHD associated fibrosis and targeting Sox9 in EVPs can reduce EndMT and fibrosis in a model of cGVHD post allo-Tx. To validate this, Cdh5-Cre/ERRosaYFP (WT) and Sox9fl/fl/Cdh5-CreERRosaYFP (Sox9 KO) recipient mice were lethally irradiated and transplanted with T-cell enriched spleenocytes of B6.SJL-Ptprca or BALB/c donor mice to generate syngeneic (syn) or cGVHD allo-Tx models, respectively. Tamoxifen was administrated at 1-week post-Tx to label endothelial cells with YFP and ablate Sox9 from the endothelium in graft recipients. Fibrotic skin was collected at 3-4 weeks post-Tx and EndMT and level of GVHD were assessed by histology and immunofluorescence staining. Reduced expression of endothelial marker CD31, increased dermal thickness, co-expression of YFP+ cells with mesenchymal marker α-smooth muscle actin (α-sma) and tansgelin (sm22a) and overall pathological inflammation score in the skin of allo-Tx as compared to syn-Tx mice reflected EndMT and fibrosis associated with cGVHD. Conditional ablation of Sox9 in endothelium reduced dermal thickness and co-expression of mesenchymal markers with YFP in the fibrotic skin of allo-Tx mice. This clearly suggest that EndMT potentially plays a role in cGVHD associated fibrosis and targeting EVPs by modulating transcription factors deciding their fate can be used as a viable therapy to improve cGVHD outcomes.