Since TNFα and IFNγ produced by Vγ9δ2 γδ T cells are thought to be the mediators of the APR and IFNγ was weakly produced in SSc patients in response to Zol (Figure 1), we examined in further detail how Zol had affected TNFα production by this patient’s (RP2) PB T cell subsets. This evidence concerns the gene IFNG and systemic sclerosis.