PURPOSE OF REVIEW: A significant number of loci implicated in rheumatoid 
arthritis (RA) susceptibility have been highlighted by genome-wide association 
studies (GWAS). Here, we review the recent advances of GWAS in understanding the 
genetic architecture of RA, and place these findings in the context of RA 
pathogenesis.
RECENT FINDINGS: Although the interpretation of GWAS findings in the context of 
the disease biology remains challenging, interesting observations can be 
highlighted. Integration of GWAS results with cell-type specific gene expression 
or epigenetic marks have highlighted regulatory T cells and CD4 memory T cells 
as critical cell types in RA. In addition, many genes in RA loci are involved in 
the nuclear factor-kappaB signaling pathway or the Janus kinase (JAK)-signal 
transducers and activators of transcription (STAT) signaling pathway. The 
observation that these pathways are targeted by several approved drugs used to 
treat the symptoms of RA highlights the promises of human genetics to provide 
insights in the disease biology, and help identify new therapeutic targets.
SUMMARY: These findings highlight the promises and need of future studies 
investigating causal genes and underlined mechanisms in GWAS loci to advance our 
understanding of RA.