Thirty-eight tissue samples from 9 patients were profiled for genome-wide DNA somatic copy number, showing consistent heterogeneous putative driver mutations, such as copy number gain/amplification of the PDGFRA, MDM4, and AKT3 loci, and deletion of the genomic locus containing PTEN. Furthermore, each tumour copy number alternations (CNA), were classified as ‘common’, ‘shared’, and ‘unique’, i.e., all tumour fragments, more than one but not all fragments, and only one fragment, having CNA respectively. The gene discussed is PTEN; the disease is neoplasm.