After ocular hypertensive injury, separate molecular mechanisms are known to contribute to RGC axonal and somal degeneration.4, 9, 30, 51, 52, 53, 54 For instance, Bax deficiency protected RGC somas, but not axons from ocular hypertension-induced RGC death.9 Furthermore, after mechanical axonal injury, we have shown that deficiency of Dlk or Jnk2 and Jnk3 protects RGCs from somal degeneration, but not axonal degeneration.18, 55 Therefore, it is possible that Jun deficiency could have an important role in somal loss in ocular hypertensive DBA/2J mice. Here, BAX is linked to hypertensive disorder.