Cancer is a genetic disease caused by the accumulation of deleterious modifications within the genome of somatic cells (1). During tumorigenesis, genomic instability leads to the progressive acquisition of silent (‘passenger’) and selected (‘driver’) mutations (2). The latter provide cancer cells with selective growth advantages that initiate clonal expansion (3). The Cancer Genome Project (CGP) has the ambitious goal of identifying all genes that are implicated in the development of cancer (4). The Cancer Gene Census (CGC) is a part of CGP and collects information on more than 370 genes whose mutations are causally related to cancer (5). Recently, high-throughput mutational screenings of several cancer types have been promoted with the aim of identifying mutated genes, without any hypothesis-driven bias. So far, four of these high-throughput experiments have been delivered. Overall, they identified 380 Candidate Cancer Genes (CAN-genes) that are mutated in breast, colorectal, pancreatic cancers and glioblastoma (6–8). Furthermore, the pilot experiment from the Tumor Sequencing Project identified 26 genes (TSP-genes) mutated in lung adenocarcinoma (9). Altogether, these studies revealed that the number of cancer genes is surprisingly high
