For example, it is hypothesized that the up-regulation of cholesterol biosynthesis in many cancers may be due to mutations in the gene transcription of SREBP2 [80], while it has also been shown that the mammalian target of rapamycin complex 2 protein Kinase B (TORC2-AKT) signalling may cancel the activation of SREBPs. This evidence concerns the gene AKT1 and cancer.