Downregulation of this stress response gene has been shown to cause mitochondrial dysfunction and ROS production that can lead to cell death.(70) Lastly, our observation that CTSL, a protein crucial for COVID-19 viral entry is upregulated across multiple cell types in severe patients provides a potential initial mechanism for the induction of the NEAT1 and MALAT1 mediated inflammatory state through increased efficiency of viral entry.(57). This evidence concerns the gene CTSL and COVID-19.