By evaluating Omicron infection on different cells, Thomas P. Peacock et al. found that the infection degree of Omicron on Calu-3 (a lung cell line, whoseTMPRSS2 expression is normal, but lack of CTSL expression, hindering the nuclear endosome pathway of virus entry) is weaker than Delta, indicating that Omicron entry is more dependent on the nuclear endosome mediated endocytosis pathway147 rather than the membrane fusion pathway involved in TMPRSS2, and TMPRSS2 is mainly distributed in human lung epithelial cells. Here, TMPRSS2 is linked to infection.