Further, our study also depicts the involvement of previously unnoticed genes such as protein kinase C-β, PRKCB (a negative regulator of BCR signaling) and cytoplasmic FMR1-interacting protein 2, CYFIP2 (inducer of p53 mediated apoptosis), which were also upregulated in all data sets and clinical RA patients (Figures 3G,H). Here, BCR is linked to rheumatoid arthritis.