Caveolae, submicroscopic bulb-shaped plasma membrane pits, are an abundant feature of many mammalian cells (Parton and del Pozo, 2013). Caveolae and the major proteins of caveolae, caveolins (Rothberg et al., 1992), and cavins (Hill et al., 2008), are linked to a number of human diseases such as muscular dystrophy, cardiomyopathy, and lipodys -trophy (see Glossary) (Bruno et al., 1993; Fernandez et al., 2006; Hayashi et al., 2009).As illustrated, caveolae show a striking tissue distribution with abundant caveolae in some cell types but an apparent absence from others. This is paralleled by highly variable expression of caveolins and cavins from tissue to tissue and the association of caveolar dysfunction with specific disease conditions (Allen et al., 2011; Bruno et al., 1993; Hansen et al., 2013; Hayashi et al., 2009).Caveolae are generated at the plasma membrane as caveolins and cavins come together to form the characteristic curved microdomain (Parton and del Pozo, 2013). They can bud from the plasma membrane, and the budded caveolae then fuse with early endosomes. The bulk of the caveolar components are then recycled back to the cell surface, but caveolae can also be disassembled and the components degraded after incorporation into the intralumenal vesicles of multivesicular late endosomal compartments (Parton and del Pozo, 2013). Caveolae at the plasma membrane can be flattened and their components dispersed in response to mechanical stress at the plasma membrane, allowing mechanoprotection or expansion of the plasma membrane (Sinha et al., 2011). Though the mechanism remains elusive, caveolae and caveolins are also known to regulate cellular signaling pathways (Garcia-Cardena et al., 1997) by direct or indirect means.