The phagocytosis of the shed tips of photoreceptor outer segments (OS) by the cells of the adjacent retinal pigment epithelium (RPE) is vital to the survival of the photoreceptor (PR) cells (Young and Bok, 1969). If this phagocytosis is inhibited, death of the PRs occurs. This situation is observed in the Royal College of Surgeons (RCS) strain of rat (Bourne et al., 1938; Dowling and Sidman, 1962). In this animal model, a recessive mutation in the receptor tyrosine kinase (RTK) genemercauses the introduction of a stop codon early in the reading frame, with the result that functional Mer protein is never produced by the RPE cells (D’Cruz et al., 2000; Nandrot et al., 2000). This mutation affects the ability of the RPE cells to perform their normal function of phagocytosing the shed tips of the OS, resulting in degeneration of the underlying photoreceptor cells, and blindness (Bok and Hall, 1971; Mullen and LaVail, 1976; Edwards and Szamier, 1977).