Other in vitro studies that showed a downregulation of BCL2 and simultaneous activation of pro-apoptotic molecules such as BAX include those by Lee et al. (role of p53 and p38 MAPK in glioblastoma cell death caused by CAPE) [103], Jin et al. (mitochondria-mediated cell death in myeloid leukemia cell lines treated with propolis) [107], and Watabe et al., who studied the inhibition of NF-κB and activation of Fas as mechanisms of apoptosis in CAPE-treated breast cancer cells [108]. The gene discussed is NFKB1; the disease is breast carcinoma.