Interestingly, Lu et al. [27] made an intriguing discovery that treatment of mouse embryonic osteoblast precursor cells (MC3T3E1 cells) with 20 ng/ml of TNF-α, simulating the effects of RA on osteoblasts, followed by treatment with varying concentrations of IL-35, resulted in a concentration-dependent promotion of MC3T3E1 cell proliferation, upregulation of VEGF and its receptor Flt-1 and Flk-1 expression, and inhibition of apoptosis [27]. This evidence concerns the gene TNF and rheumatoid arthritis.