A favorable effect on amyloidosis can be expected in RA and AS patients since TNF-α is a strong inducer of inflammation in these diseases,[37] SAA was suggested to be a good marker of RA disease activity, and SAA levels were decreased with anti-TNF treatment in RA patients.[38] However, the experience with anti-TNFs in patients with FMF was extremely limited.[39] We observed a similar outcome with anti-TNFs in our AA amyloidosis patients with and without FMF. This evidence concerns the gene SAA1 and rheumatoid arthritis.