Whilst, in normal conditions, TET2 modulates the expression of SRF, allowing for the VSMCs between synthetic and contractile states, the hypertension-related downmodulation of TET2 [56] leads to a reduced response to vascular injury, and when VSMCs switch to the contractile state, this leads to the hyperacetylation of H3 and H4 on the smooth muscle cell 22 (SM22) [66] and myocardin genes by SRF. This evidence concerns the gene SRF and hypertensive disorder.