Mouse models have demonstrated that the targeted knockout of both TP53 and RB1 genes can induce tumors that closely resemble human SCLC.[57] Furthermore, the deletion of TP53 and RB1 contributes to chemotherapy resistance in tumor cells, significantly impairing treatment efficacy.[58] Recent studies have highlighted the pivotal role of TP53 in maintaining cellular iron metabolism through the regulation of ferritin synthesis and degradation. Here, TP53 is linked to neoplasm.