JUN and cancer: Signaling in wound healing is remarkably similar to cancer, often activating Receptor Tyrosine Kinases like the Epidermal Growth Factor Receptor (EGFR)-RAS-MAPK axis that lead to transcription of Immediate Early Genes like c-FOS or c-JUN, inhibition of epigenetic repressors like the Polycomb Group (PcG), and loss of H3K27me3 inhibitory epigenetic marks (11, 20).