Clonal genomic alterations shared by components of a mixed tumor have been observed in key SCPC genes such as TP53 [15], and are capable of driving gene expression changes despite maintenance of morphology; for instance, gene expression changes intermediate to SCPC were recently reported in a xenograft model of transdifferentiation derived from a primary prostatic adenocarcinoma with bi-allelic alterations in TP53, RB1, and PTEN [12, 36]. This evidence concerns the gene PTEN and prostate adenocarcinoma.