?Non-arteritic anterior ischemic optic neuropathy (NA-AION) is one of the major causes of blindness or seriously impaired vision in aged people over 55 years old. NA-AION clinically presents with painless loss of vision in the affected eye, ON swelling (disc edema), and disruption of the normal nerve architecture, resulting in RGC death through apoptosis and permanent vision loss. The retrospective study reported by Hayreh and Zimmerman showed that the systemic steroid treatment was effective in patients with NA-AION, of whom the initial visual acuity 20/70 or worse and seen within 2 weeks of onset (Hayreh and Zimmerman, 2008 b). The report brought more debate about “should we put systemic steroid in the first line of treatment for NAION?” On the other hand, the characteristic high spontaneous improvement rate of NA-AION (41%) not only making clinical studies easily fall into bias, but bringing difficulty in design a prospective study. The other interesting treatments for the past decade were the role of neuroprotection in NA-AION. Disappointingly, levodopa, carbidopa and 0.2% brimonidine failed to provide beneficial effect. Other clinically uncontrolled reports showed promising results; those treatments included intravitreal injection (IVI) of triamcinolone (TA), IVI of bevacizumab and IVI of erythropoietin. However, these reports were experimental; a few larger confirmatory pre-clinical studies are required before an expensive randomized controlled trial can be attempted.