We previously identified cell surface markers associated with repression of p16(INK4a)/cyclin-dependent kinase inhibitor 2A(CDKN2A), a critical determinant in the acquisition of a state in which cells can choose various fates, i.e. a “plastic” state. These cell surface markers allowed us to isolate rare cells from healthy human breast tissue that exhibit extensive lineage plasticity. We referred to these cells as “Endogenous Plastic Somatic (ePS) cells”. These cells express canonical plasticity markers, OCT3/4, SOX2, and NANOG, at levels similar to those measured in human embryonic stem cells and to acquire a plastic state sensitive to environmental programming. However, in contrast to other cells that express OCT3/4, SOX2, and NANOG, ePS cells are mortal, express low telomerase activity, expand for a finite number of population doublings, and maintain a diploid karyotype before arresting in G1. In this more recent study, we visualized ePS cells in breast tissue sections. We also characterized ePS cells in a non-plastic (latent) state in which they do not express plasticity markers OCT3/4, SOX2, and NANOG and in a plastic state in which they express these plasticity markers. Moreover, we identified the signaling pathways required for the acquisition of plasticity markers OCT3/4, SOX2, and NANOG in latent ePS cells.