Current mechanistic evidence is largely centred around ACE2, nicotinic acetylcholine receptors (nAChRs) and RAS, with potential crosstalk between ACE2 and nAChRs via RAS implicated in both reduction of SARS-CoV-2 infection [12, 16, 17] and more severe COVID-19 through stimulation of inflammatory signalling pathways [18–20]. Here, ACE2 is linked to COVID-19.