We interpret these findings such that this tumor is exclusively driven by the loss of CDH1 and gain of CCND1. Otherwise, one would have expected that other, for tumorigenesis beneficial gains and losses, for instance the gain of COX2 or the loss of TP53, which are present in minor clones of 10S, would have become major clones under the selective pressure. The gene discussed is TP53; the disease is neoplasm.