Despite the fact that enhanced ECM contraction and adhesion observed in SSc fibroblasts depends on TGFβ type I receptor (ALK5) activity, the fundamental mechanism underlying the contribution of TGFβ to the fibrotic phenotype of SSc is unclear as, in this cell type, ALK5 inhibition was unable to reduce critical features of the myofibroblast phenotype, such as α-SMA expression and stress fibre formation [10]. The gene discussed is ACTA1; the disease is systemic sclerosis.