Other mechanisms explaining over activation of mTOR involve the loss of regulatory inhibitory gene activity of the tuberous sclerosis complex (TSC) proteins or PTEN inactivation by methylation of the promoter, gene mutation, or allelic deletions such as those reported in perivascular epithelioid cell tumors (PEComas). This evidence concerns the gene MTOR and neoplasm with perivascular epithelioid cell differentiation.