CCL3L3 and rheumatoid arthritis: The WTCCC specifically examined three loci within which CNV had been implicated in auto-inflammatory disease (CCL3L1, β-defensin, FCGR), and were unable to replicate previous reports of association with disease [3–5,7], although there was a nominal P = 0.058 for association of CCL3L1 with rheumatoid arthritis, in a direction of association consistent with that previously reported [4].