Studies have reported that HDAC can contribute to SARS-CoV-2 pathogenicity in several ways – i) HDAC upregulates ACE2 expression and promotes viral entry to the cells [107], ii) HDAC activates pro-inflammatory responses against viral infections and may give rise to CS [108] iii) HDAC activity accumulates Acetyle Co-A, which elevates the cholesterol level [109]. This evidence concerns the gene ACE2 and Cowden syndrome 1.