Cell death induced by both agents occurred due to prolonged ER stress, ATF4/CHOP pro-apoptotic function simultaneously with Rad51 downregulation and Ataxia Telangiectasia Mutated/Checkpoint kinase 2 (ATM/CHK2) activation, resulting in irreversible DNA damage and tumor doubling delay in vivo (Figure 3) [152]. This evidence concerns the gene ATF4 and neoplasm.