Epithelial plasticity can lead to classical EMT (loss of cell-cell and cell-substratum attachments, new actin rearrangements, and gain of mobility) or reversible scatter, which looks like EMT but is not enduring and can revert. These events are regulated by ligand-inducible intrinsic kinase receptors on the cell surface, which modulate small GTPases, Smads, PI3Ks, MAP kinases, and the availability of β-catenin to coactivate LEF in the nucleus. Free levels of b-catenin are regulated by E-cadherin or APC/β-catenin/Axin complexes, the latter of which shuttle b-catenin between ubiquination or utilization in adherens junctions. Activation of nuclear transcription provides new transcriptional regulators (Snail, SIP1, Ets, and FTS-BP/CarG box binding factor) of the EMT proteome. The EMT proteome comprises proteins listed in Table 1. The variability of receptors, kinases, and the emergence of combined preferences for signaling pathways determine the plasticity unique to each epithelium.