The occurrence of patients with TSC-LAM is caused by mutations in the TSC1 or TSC2 genes.[3] LAM occurs more frequently in patients with S-LAM, and patients with S-LAM can be caused by mutations of the TSC2 gene.[4] Mutations in these genes result in the dysregulation of the mammalian target of the rapamycin mTOR pathway.[5]. This evidence concerns the gene MTOR and lymphangioleiomyomatosis.