Lymphangioleiomyomatosis (LAM) is a devastating pulmonary disease caused by mutation of tuberous sclerosis complex 1/2 (TSC1/2), resulting in mammalian target of rapamycin complex 1 (mTORC1) activation [1], which chiefly affects young women of childbearing age [2]. Here, TSC1 is linked to lymphangioleiomyomatosis.