Additional studies of experimental glaucoma models are needed for further characterization of the JNK-mediated RGC death signaling; however, it is evident that various pathogenic processes implicated in glaucomatous neurodegeneration, including distortion of axonal cytoskeleton, neurotrophin insufficiency, mitochondrial dysfunction, metabolic failure, endoplasmic reticulum stress, or inflammatory signaling, can activate JNKs, as detected in human glaucoma and animal models [139,140,146,147,148]. This evidence concerns the gene BDNF and glaucoma.