It has been progressively recognized that several oncogenic pathways are closely associated with ferroptosis.100 For example, most KRAS mutation-driven pancreatic cancers are sensitive to ferroptosis activators, Erastin.101,102 Furthermore, new evidence suggests that as cancer suppressor gene, p53 inhibits cyst(e)ine uptake and sensitizes cells to ferroptosis by suppressing the expression of Xc-system.81,103,104 However, it has also been shown that p53 can limit Erastin-induced ferroptosis in a transcription-independent manner by blocking dipeptidyl peptidase-4 (DPP-4) activity.105. This evidence concerns the gene DPP4 and pancreatic neoplasm.