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). This evidence concerns the gene TP53 and rheumatoid arthritis.