Laniosz et al found that BPV-1 although shown to possess the entry capacity via clathrin-dependent endocytosis, was incapable of establishing an infection without caveolin-1, suggesting that the virus whose entry was facilitated via clathrin-mediated endocytosis, utilized the caveolar pathway postentry for infection, where the Rab 5 might induce or be involved in its transport from the endosome to the caveosome (Fig. 1D) [38]. The gene discussed is CAV1; the disease is infection.