In animal models, intranasal infection with mouse‐adapted SARS‐CoV‐2 induced loss of DA neurons in the substantia nigra at 120 days post‐infection,156 and intranasal infection of transgenic mice with ubiquitous human ACE2 expression (AC70‐hACE2) reduced expression levels of the D2 dopamine receptor and tyrosine hydroxylase (TH), the rate‐limiting enzyme involved in DA synthesis.159. The gene discussed is TH; the disease is infection.