In this scenario, the bis-aryl urea derivative N69B demonstrated its anticancer activity by increasing cathepsin D-mediated tumor cell apoptosis through the B-cell lymphoma 2 (Bcl-2) homology domain 3 interacting domain-death agonist (Bid)/Bcl-2-like protein 4 (Bax)/cytochrome C/caspase 9/caspase 3 pathway activation [47]. This evidence concerns the gene BAX and neoplasm.