Nevertheless, an anti-TNFα antibody locked with a peptide cleavable by MMP2/9 showed therapeutic effects equivalent to unmodified anti-TNFα in a mouse model of rheumatoid arthritis, but animals treated with MMP2/9 activable pro-drug lacked the systemic immunodepression secondary effects that animals receiving the unmodified antibody showed [29]. The gene discussed is MMP2; the disease is rheumatoid arthritis.