Through up-regulating SREBP1 transcription, processing and nucleic accumulation, mTOR signaling senses nutrients for growth and accelerates de novo lipogenesis.42 In particular, Calvisi has reported that AKT-mTORC1 signaling-induced lipogenesis accelerated HCC development from transcriptional and post-transcriptional aspects, including downregulation of FASN ubiquitination and interruption of SREBPs degradation.40 Consistently, in our study, SREBP1 was revealed to be upregulated by TIP30 deficiency-mediated Akt/mTOR activation. The gene discussed is HTATIP2; the disease is hepatocellular carcinoma.