Those results support the hypothesis put forward by Miller et al. [98], that in NAD+-deficient COVID-19 patients, due to either advanced age, obesity or type 2 diabetes mellitus (T2DM), SIRT1 activity is compromised and unable to downregulate ADAM17 (a disintegrin and metalloproteinase domain 17, also known as TNF-α-converting enzyme) and restrict uncontrolled increase in TNF-α and IL-6. The gene discussed is ADAM17; the disease is COVID-19.