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 small cell lung carcinoma.