As a result, there is less remaining undeamidated 4E-BP2 available to inhibit the overproduction of pathological precursors of neurodegenerative diseases (Step B), namely tau (Option 1), Aβ (Option 2), and α-synuclein (Option 3), as well as mitochondrial dysfunction (Option 4), which inhibits mitophagy (4a) and produces mitophagy dysfunction- inducing reactive oxygen species (ROS, 4b) that cause oxidative stress, which also inhibits mitophagy. Here, EIF4EBP2 is linked to neurodegenerative disease.