S1PR3 and lymphangioleiomyomatosis: 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.