Verjee et al.13 demonstrated that tumour necrosis factor (TNF) treatment for palmar dermal fibroblasts derived from patients with Dupuytren’s disease led to activation of Wnt/β-catenin signalling through GSK-3β phosphorylation and inhibition, resulting in upregulated COL1 and α-SMA expression. This evidence concerns the gene GSK3B and Dupuytren Contracture.