In LAM cells, the loss of heterozygosity (LOH) in the tuberous sclerosis complex (TSC) 1 or TSC2 tumour suppressor genes, which code for hamartin and tuberin, respectively, leads to the hyperactivation of mammalian Target of Rapamycin Complex1 (mTORC1) for the absence of one of the two proteins [7]. Here, TSC2 is linked to neoplasm.