Humans are composed of a hundred million million cells. Each cell may start to divide, or continue to divide, when it should not. The relentless division leads to a tumor, and when cells of the tumor take residence at a location they should not, the result is cancer. Lesions (i.e., mutations) in our genetic material are known to be the basic cause of cancer formation. These mutations convert regular genes into cancer genes, which drive the proliferation of a cell and its potential to metastasize. But because cells differ, the corresponding cancers also differ, and so it is important to map these differences for diagnosis and treatment.

Tumors in small animals such as mice are cured relatively easily because tumor mass is small and few, if any, cells with mutations other than those of the main tumor mass (i.e. mutants) have accumulated. In humans, however, tumor mass is large at the time of discovery, and the number of pre-existing mutants is much higher. Those cells that may have mutated out of the therapeutic range of a drug are responsible for one of the biggest problems in cancer treatment: the relapse. It follows that the most cogent cancer treatment would target as many cancer gene products as possible, thereby targeting cancer cells within a single tumor that manifest diverse resistance mutations. Knowledge of all active cancer genes in a particular tumor, along with the position of their products in the biological pathways, will be necessary for a true cure.