Laboratory investigations were unremarkable, including blood lead level, cerebrospinal fluid (CSF) routine and biochemistry, autoimmune encephalitis antibody panel (NMDAR, AMPAR1/2, LGI1, CASPR2, GABABR, IgLON5, DPPX, GAD65, GlyRα1, mGluR5, and D2R in both serum and CSF), cerebellar ataxia–related antibodies (GAD65, Homer3, ARHGAP26, ATP1A3, CARP VIII, NCDN, GluRδ2, CASPR2, PCA2, Yo, mGluR1/2/8, and KLHL11 in serum and CSF), and paraneoplastic neuronal antibody panel (Hu, Ri, CV2, Ma1/2, amphiphysin, GAD65, Tr, Zic4, PKCγ, and SOX1 in CSF). Here, GAD2 is linked to aceruloplasminemia.