In a human sequential lung cancer development scheme, early events such as loss of heterogeneity, microsatellite alteration, and small telomeric deletions precede morphological abnormalities (e.g., hyperplasia, dysplasia, and carcinoma in situ) and mutations of key genes such as Egfr, Plau, p53, and Kras [46,47]. This evidence concerns the gene TP53 and in situ carcinoma.