(A) As judged by a validated grading scale of optic nerve damage29, the distribution of optic nerve damage in D2.Bim-/- mice was significantly different to D2.Bim+/+ (P<0.001) at 12 months of age. D2.Bim+/? (wild-type and heterozygous mice were included in the analysis; no difference in optic nerve degeneration was noted between the genotypes) had a similar profile of optic nerve damage to previous reports3,8,29: 33 nerves assessed with 36% no or early, 9% moderate, 55% severe. In contrast in D2.Bim-/- eyes there were far fewer nerves judged to have severe optic nerve damage (41 nerves assessed, 53% no or early, 32% moderate, 15% severe). (B) To determine if Bim deficiency protected RGC somas after glaucomatous injury ganglion cell layer neurons were counted in D2.Bim+/+ and D2.Bim-/- eyes. For both genotypes, eyes with corresponding optic nerves judged either without damage (no or early) or severe were counted. Note, only RGCs die in DBA/2J glaucoma35 and approximately half of RGC layer neurons are amacrine cells32,34, so a loss of 50% of ganglion cell layer neurons equals complete RGC loss. Bim deficiency did not prevent somal loss in glaucoma. N≥5 for both genotypes and grades. Scale bar, 100 μm.