While previous platelet transcriptomic studies in COVID-19 patients did not specify the type of variant,9,10 a study involving mice expressing human ACE2 analyzed transcriptomic changes in MKs upon infection with Delta variant and found that processes such as histone modifications, MK differentiation and NETosis were affected in the MKs of COVID-19-infected mice.13 Notably, our findings suggest that the Delta variant was the most proinflammatory, characterized by significant upregulation of interferon and ISGylation signaling pathways and hypercytokinemia. The gene discussed is ACE2; the disease is COVID-19.