It has previously been suggested that the mitochondrial pathway takes a center-role in iron chelator-mediated cell death since over-expression of anti-apoptotic Bcl-2 and Bcl-XL promotes cell (in HeLa cervix carcinoma cells) survival and chelator-mediated cell death can be blocked by a dominant-negative caspase 9 and Bcl-XL over-expression [71]. This evidence concerns the gene BCL2L1 and cervical carcinoma.