They also suggest, a possible connection between the upregulated DPYSL3 and TNF-α, where DPYSL3 is supposed to affect the repair of damaged bone, through the bone morphogenetic protein (BMP) and ras homolog gene family member A (RhoA) signaling.73 Some additional new evidence proposes, that the PI3k/Akt pathway might be indeed implicated in the pathogenesis of RA but not EV mediated. This evidence concerns the gene DPYSL3 and rheumatoid arthritis.