Endogenous and environmental ligands bind to NHRs to activate nongenomic signaling and kinase cascades. Activated kinases such as AKT and PKA phosphorylate and inhibit the activity of epigenetic “writers” such as the HMT EZH2 and “readers” such as HP1γ respectively. The “eraser” HDM PHF2, also a PKA substrate, becomes activated when phosphorylated. In all three scenarios, the result is increased gene expression, due to loss of, or inability to read, repressive histone methyl marks.