Mammary cell lines overexpressing various EMT-TFs showed PLCγ-mediated PKC activation leading to a c-Jun/Fra1-induced CSC transcriptional program.82 TGF-β and TNFα pathways interact to drive both EMT and upregulate breast CSC properties.83 Elegant in vitro and in vivo studies in a Trp53-null mouse breast cancer model showed cross-talk between transformed mesenchymal cells and tumor-initiating subpopulations. The gene discussed is JUN; the disease is neoplasm.