Considering the critical role of SPHK1/S1P/S1PR3-regulated autophagy in the progression of cancer [12, 13], we hypothesize that abnormal sphingolipid metabolism may be exploited as a novel therapeutic target in LAM treatment and that leveraging sphingolipid metabolism combined with mTORC1 inhibitor treatment may improve therapeutic strategies for LAM, TSC, and related diseases. The gene discussed is SPHK1; the disease is lymphangioleiomyomatosis.