Recently, 3-iodothyronamine (T1AM), an endogenous thyroid hormone (TH) derivative, able to interact directly with a specific G-protein coupled receptor known as trace amine-associated receptor 1 (TAAR1) [14,15], has gained interest for its ability to promote neuroprotective effects in several models, including seizure-related excitotoxic damage, altered autophagy, amyloidosis, and OGD-induced synaptic dysfunction [16,17,18,19], and to efficiently cross the blood–brain barrier (BBB) [20]. The gene discussed is TAAR1; the disease is amyloidosis.