A line of rats with hereditary kidney cancer were developed by Japanese researchers. They have a mutation in the FLCN homolog that produces a truncated protein, though they do not develop the cutaneous or pulmonary symptoms seen in humans. Heterozygotes have renal abnormalities seen very early in life that develop into clear-cell and hybrid tumors, significantly shortening the animals' lifespans; they also are prone to endometrial and salivary gland clear-cell hyperplasia as well as rhabdomyolysis. Homozygotes do not survive to birth. When a wild-type FLCN gene was added, the phenotype was rescued.
