Examination of pathways, transcription factors, and cluster gene expression data (Fig. 5c, e, f) support an initiating/driving role of Tr2 through gene expression, including EZH2 and RBL1, and upregulation of cell cycle and cell division, tumor development for Tr5 through LEF1 and PTCH1 expression and increased morphogenesis and development, loose support for endothelial nature of Tr4 through DLK1, FLT1, and VIM signaling, and tumor maintenance for Tr3 through strong metabolic signature and EGFR and IGFBP2 expression. The gene discussed is VIM; the disease is neoplasm.