The invading cell in LAM develops from an unknown source and carries mutations in the tuberous sclerosis complex (TSC) genes that cause constitutive activation of the mechanistic target of rapamycin (mTOR) pathway, disrupted cellular proliferation, and a program of unsuccessful lymphangiogenesis due to which there is a characteristic aberrant smooth muscle-like cells infiltrating the lung parenchyma and causing cystic lung damage. [1]. Here, MTOR is linked to lymphangioleiomyomatosis.