In addition, whether the SARS-CoV-2 co-receptor NRP1, which when co-expressed with ACE2 and TMPRSS2 enhanced virus entry and infection [73,69], contributes to the mechanisms of virus endocytosis is an interesting subject for further studies, in particular, since NRP1 is reported to be internalized via both clathrin-dependent endocytosis involving SH3BP4 and GIPC1 binding [80], but also dynamin-independent endocytosis [81,82]. Here, DNM1 is linked to infection.