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An alternative oxidative pathway for EE that has been identified is removal of the ethinyl group (from EE or its metabolites), which then renders E1 or E2 metabolites, with significant formation of 2-hydroxyestrogens 34

TBX3 played a key role in regulating cellular senescence by repressing p14 ARF expression through interactions with histone deacetylases (HDACs), and by inhibiting p16 INK4a either through suppression of cyclin-dependent kinase activity or by cooperating with the polycomb protein EZH2 to promote its epigenetic silencing [45, 46]

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These findings reinforce the clinical evidence that ASD is associated with an abnormal inflammatory response