Molecular docking implicated tumor necrosis factor-α (TNF-α; PDB: 2AZ5) as a putative target: 18b formed a stable complex featuring hydrogen bonds and complementary noncovalent contacts within the cytokine interface, consistent with the proposed mechanism wherein TNF-α signaling can promote breast-cancer progression (e.g., via aromatase upregulation). This evidence concerns the gene CYP19A1 and breast carcinoma.