For example, it would be interesting to address whether SIRPα/β is also a genetic risk loci associated with ADA development in patients with RA, and whether the low frequency of SIRPα/β+memory B cells in RA patients prior to adalimumab treatment is exclusively a biomarker for ADA response or whether the reduction of this population is also mechanistically implicated in the development of an ADA response. Here, ADA is linked to rheumatoid arthritis.