Early phylogenetic separation of these genetically different tumor cell subpopulations was further supported by a STAT2 mutation as well as whole genome doubling (WGD) exclusive to area B and the metastases, while area A and the in situ area instead harbored a heterozygous truncating ARID1A mutation and a YAP1 amplification (Fig. 4b, c). The gene discussed is ARID1A; the disease is neoplasm.