Then, the SASP amplifies senescence effects in a paracrine way to non-ACE2 expression cells, which contributes to the pathological changes in the lungs, including excessive release of pro-inflammatory cytokines, endothelial cell damage, aberrant neutrophil activation, fibrosis, and microthrombosis, all of which are associated with severe COVID-19 outcomes (Schmitt et al. 2023). This evidence concerns the gene ACE2 and COVID-19.