With this in mind, one could postulate that while TSC gene mutations in NSCs lead to the CNS lesions, mutations within the neural crest lineage are responsible for the development of most other TSC lesions, including those associated with LAM, and that variable mutational burden within the neural crest (NC) lineage leads to the greatest heterogeneity in TSC disease phenotypes. This evidence concerns the gene SLC12A3 and lymphangioleiomyomatosis.