That TF-1 induction in the setting of exposure to Zol can be blocked by an anti-TNFα antibody even in the presence of enhancement by patient’s plasma (Figure 5) suggests that TNFα released by Zol-activated Vγ9δ2+ T cells plays a major role in induction of TF-1 and that anti-TNFα mAb could be used to prevent thrombosis in high risk SSc patients treated with Zol. The gene discussed is TNF; the disease is systemic sclerosis.