The Omicron variant appears to be less dependent on TMPRSS2 and has a preference for endocytic entry, where cathepsin carries out S2′ cleavage within endosomes.2 In addition, we have observed a cleavage defect in virus producer cells and impaired cell-cell fusion.2 Given the broad expression of ACE2 across diverse tissues, it is unsurprising that infection of multiple organs occurs during COVID-19 infection. The gene discussed is ACE2; the disease is infection.