Indeed, in a KrasG12D lung cancer model, KrasLSL-G12D/+; Trp53+/−; mir-34a−/− mice exhibited increased tumor area and the number of high-grade tumors than KrasLSL-G12D/+; Trp53+/− mice, suggesting that mir-34a deficiency accelerated tumor progression when p53 response is compromised [19]. This evidence concerns the gene TP53 and lung carcinoma.