Consistently, geniposide attenuated the expressions of Bax and TLR4, caspase-3 cleavage, and the phosphorylation of p53, while increasing Bcl-2 expression, suggesting that the antiapoptotic property of geniposide is due to its modulation of TLR4 and apoptosis-related factors (p53, Bax, Bcl-2, and caspase-3) in LPS-induced mouse mastitis [74]. The gene discussed is BAX; the disease is mastitis.