The evidence of an altered lipid metabolism in tuberin-null cells, e.g., involving LPCs and GD3, and the demonstration of metabolic abnormalities in LAM patient serum, mainly LPCs, sphingolipids, phospholipids and acylcarnitine fatty acids, provides the need to promote the comprehension of lipid dysmetabolism in LAM as novel biomarkers for a metabolic signature for stratifying LAM patients and to suggest useful therapeutic targets, also to associate to mTOR inhibitor rapamycin, for the treatment of LAM. The gene discussed is MTOR; the disease is lymphangioleiomyomatosis.