The understanding gained regarding the molecular pathology of cancer in recent decades suggests that some tumor types exhibit stand-alone recurrent genetic aberrations, such as chromosomal translocations, that result in gene fusions, e.g., SYT-SSX in synovial sarcoma (SS) [3], TLS-CHOP in myxoid/round cell liposarcoma (MLS) [4], and KIF5B-RET in lung adenocarcinoma [5], or somatic mutations, e.g., KIT in gastrointestinal stromal tumors (GIST) [6] and 26 mutated genes (TP53, KRAS, EGFR, and 23 other genes) in lung adenocarcinoma [7]. The gene discussed is TP53; the disease is lung adenocarcinoma.