We show here that the exclusive down-regulation of Bcl-2 expression (in contrast to unmodified Bcl-XL or Bid) takes a center role in the pro-apoptotic response of SKOV-3 cells to treatment with HNTMB. Similarly, other AHC compounds and their iron complexes cause apoptosis via the mitochondrial pathway (in Jurkat T cells and K562 leukemia) which could be counteracted by Bcl-2 overexpression [73]. This evidence concerns the gene BCL2 and leukemia.