The mitochondrial donor AP39 reduced infarct size, reactive microglial activation, and pro-inflammatory markers such as ionized calcium-binding adapter molecule 1 (Iba1), IL-1β, IL-6, and TNF-α, as well as the proneurotrophin growth factor-p75 neurotrophin receptor/sortilin/caspase-3 (proNGF–p75NTR–sortilin/caspase-3) axis, while inducing neuroprotective BDNF–tropomyosin receptor kinase b (BDNF–TrkB) and nerve growth factor-tropomyosin receptor kinase a (NGF–TrkA) signaling during cerebral ischemia [105]. The gene discussed is NTRK2; the disease is brain ischemia.