Although a high frequency of elevated inflammatory markers was observed in our TA patients, as well as a negative correlation between CRP with HDL-c, similar to found in lupus [2], the absence of a reactivity to lipoprotein lipase suggests that anti-LPL antibodies are not implicated in the ongoing active complex inflammatory process causing vascular damage in TA. The gene discussed is CRP; the disease is systemic lupus erythematosus.