Using this methodology, Su and colleagues analyzed two patients, showing consistent intercell variability in mutations: one these patients showed a classical linear evolutionary profile, while the other showed early tumor branching; thus, in the first patient, all the cells shared the same TP53 mutation, implying a monoclonal origin, while in the second patient, only a subpopulation of cells contained the TP53 driver mutation, while other cells carried different driver mutations, supporting a polyclonal origin of prostate cancer [42]. This evidence concerns the gene TP53 and neoplasm.