Functionally, chemoresistance has been linked to HO-1: replicon models with HO-1 overexpression resist oxidant-induced cytotoxicity [35,36], and across malignancies (renal, prostate, pancreatic cancers, melanoma, lymphosarcoma, hepatoma) HO-1 upregulation is tied to progression and treatment resistance [56,57,58,59]. This evidence concerns the gene HMOX1 and pancreatic neoplasm.