Studies have shown that loss of tumor suppressors (e.g., p53 and BAP1), mutations in proto-oncogenes (e.g., KRAS) or overexpression of pro-tumor function proteins (e.g., OTUB1) increase the levels of SLC7A11 by upregulating its transcriptional levels or stabilizing its protein, thereby suppressing iron death and promoting tumor development (Koppula, Zhuang & Gan, 2021). This evidence concerns the gene KRAS and neoplasm.