We [2], along with Leung et al. [3], have shown that ACE-2 expression is upregulated in the small airway epithelia of smokers and patients with COPD. In particular, we observed increased ACE-2 expression in type-2 pneumocytes and alveolar macrophages along with the small airway epithelium of smokers compared to healthy never-smokers [2]. Similar studies are yet to be done in the context of electronic cigarettes (e-cigarettes), heat-not-burn devices (IQOS) or waterpipe exposure to human airways. ACE-2 is the binding site for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), mediating entry of the virus into cells [4]. Binding affinity between the spike proteins of the virus and ACE-2 on respiratory cells has been identified to be much higher than any previously identified human coronavirus. The significance of such overexpression of ACE-2 in smokers should not be ignored. COVID-19 and progression of severe pneumonia may be more likely to occur in smokers, particularly in those that have smoking-related comorbidities [5]. We are beginning to elucidate the role of traditional cigarette smoking and nicotine-driven changes to the lungs in the context of coronavirus transmission and susceptibility. Cigarette smoke has been identified and linked to increasing expression of the binding site for the cause of the 2020 pandemic (SARS-CoV-2) via mediating nicotine receptors. With this, an avoidable and potentially gigantic risk-factor has emerged for COVID-19, as the pandemic continues to claim ultimate grasp over the year of 2020.