The p73 is one of three transcription factors that belong to p53 family. The p73 is important for normal development of nervous system and has a significant role in cancer development. Unlike p53 it is rarely mutated in cancer, and mutations lead to developmental defects but not to tumor formation. The main mechanism of p73-dependent carcinogenesis involves alterations in expression of multiple isoforms that are formed due to transcription from the second promoter and an alternative splicing. The p73 isoforms may act as tumor suppressors or oncogenes, depending of the presence of the N-terminal trans-activation domain, which controls the transcriptional activity. Transcriptionally active isoforms can bind the same responsive elements as p53 due to high similarity of their DNA-binding domains and activate transcription of the same target genes including genes that encode pro-apoptotic and anti-proliferative proteins. The mechanism of p73 expression regulation is complex and still poorly understood, being affected by many stress signals and mediated by alteration in transcription, alternative splicing, proteasomal degradation. p73 levels were recently found to be regulated by mTOR, a key protein that tunes up cell metabolism. mTOR functions as a component of two alternative protein complexes mTORC1 and mTORC2. An inhibition of mTOR results in an up-regulation autophagy and inhibition of cell growth. The mTORC1 inhibitor rapamycin was shown to increase p73 level, and we tested whether Torin-2, the recently described potent inhibitor of both mTORC1 and mTORC2 might also affect p73 expression. Indeed, treatment of HCT116 cells with Torin-2 elevates expression of transcriptionally active p73 isoforms with N-terminal trans-activation domain and does not affect the level of N-truncated p73 isoforms. The result suggests that p73 may play a role in fine-tuning cell responses to metabolic stresses.