Defects in the TSC1/TSC2 complex, an inhibitor of the mammalian target of rapamycin pathway, result in TSC, a congenital condition.[10] The majority of individuals (around 80%) are diagnosed during childhood, although in rare cases, the usual neurological symptoms and skin characteristics may not present until late childhood or adulthood, delaying the diagnosis.[11] In addition to improving treatment outcomes and reducing needless medical expenditures, early detection can improve the prognosis for people with TSC. This evidence concerns the gene MTOR and tuberous sclerosis.