While the tumor expectedly grew intensely until the end of the experiments in the animals treated with Δ4-androstenedione (Δ4A, the substrate of the aromatase making estrogen), the proliferation of cancer cells originally treated with Δ4A and, then, with DHED slowed down to a level close to what was seen in the vehicle or DHED-alone treatment groups. This evidence concerns the gene CYP19A1 and neoplasm.