Preliminary findings were against this theory; some authors looked for expression of ACE2 and TMPRSS2 first in mice [37], and then in human olfactory sensory tissue by collecting biopsies via nasal endoscopic surgery; the results demonstrated that olfactory sustentacular cells expressed ACE2 and TMPRSS2, rather than olfactory sensory neurons suggesting that neurological manifestations as anosmia are due to inflammation of non-neuronal cell types in the olfactory epithelium [38]. Here, ACE2 is linked to Kallmann syndrome.