A number of models have been proposed to describe the function of Ifitm3 in providing resistance to cellular infections including building a protein lattice in the membrane to block endosomal exit, blocking fusion pores during virus-endosome hemifusion, enhancing the deposition of cholesterol to also block virus exit or by blocking virus entry by enhancing the stability of the clathrin/vATPase complexes on the endosomal membrane [13–15]. Here, IFITM3 is linked to infection.