However, data are limited and this remains an area where no consensus exists, requiring more evidence.[8] According to Bajaj et al, the activation of mammalian target of rapamycin signaling as a result of mutations or deletions of tuberous sclerosis genes (TSC1 or TSC2) is a key molecular driver of PEComa. The gene discussed is MTOR; the disease is neoplasm with perivascular epithelioid cell differentiation.