Previous reports that Ha-Ras proto-oncogene intersects with TGFβ signalling events in several fibrotic conditions [8,9], together with recent evidence that scleroderma auto-antibodies stabilize Ha-Ras levels through ROS action [15,16], led us to hypothesize that increased Ha-Ras activity may influence TGFβ signalling during the early phase of the pro-fibrotic response. The gene discussed is TGFB1; the disease is scleroderma.