Homozygous deletion of FLCN in mice resulted in early embryonic lethality; FLCN heterozygous knockout (FLCN+/−) mice appeared normal at birth, but developed kidney cysts and solid tumors, as they aged, of different histologic types (oncocytic hybrid, oncocytoma, and clear cell carcinoma with concomitant loss of heterozygosity of FLCN); these tumors displayed increased mTORC1 and TORC2 activity [112]. The gene discussed is FLCN; the disease is clear cell adenocarcinoma.