Our study supports this contention and provides insights into the mechanisms that may underlie these associations by demonstrating that the levels of circulating CHI3L1 increase during murine aging, that these inductive events are abrogated by treatment with anti-CHI3L1, and that CHI3L1 stimulates ACE2 and SPP, which increases ACE2-S protein-cell interaction, S protein activation, and pseudovirus-S infection. The gene discussed is CHI3L1; the disease is infection.