The shifted Th1/Th2 equilibrium (in favour of Th1 cells) increases the levels of IFNγ directly [19] rather than indirectly as a result of cross-talk between the type-I and type-II IFN signalling pathways eg) via type-I interferon mediated activation of STAT1 homodimers, which are the primary means of signalling from IFNγ [20] and have recently been shown to be associated with SLE in a Swedish cohort [21]. This evidence concerns the gene STAT1 and systemic lupus erythematosus.