Abstract
Tuberous sclerosis complex (TSC) is an autosomal dominant multisystemic disorder.1 Pathogenic variants in TSC1 or TSC2 gene lead to hyperactivation of the mammalian target of rapamycin (mTOR) signaling pathway, with a consequent deregulation of cell growth and the development of hamartomas. This tumors are benign, but they can cause life-threatening hemorrhage or organ failure in vital organs, such as the kidney, with angiomyolipoma (AML).1 AML found in 60% to 80% of patients with TSC are tumors composed of smooth muscle-like cells, adipocyte-like cells, and epithelioid cells.
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