NRF2是一种转录因子，在癌症形成中发挥关键作用，通过与多个促生存途径的相互作用来实现。 NRF2控制解毒酶的转录和多种其他分子，这些分子涉及到几个关键生物学过程。本文将重点探讨NRF2与STAT3之间的复杂相互作用，后者通常在癌症中被异常激活，驱动肿瘤形成和免疫抑制。 ER应激/UPR激活可以调节NRF2和STAT3，它们之间的相互作用受到自噬和细胞因子的影响并产生影响，有助于塑造微环境，并通过调节热休克蛋白的表达来控制DDR的执行。鉴于这些转录因子的重要性，更多的研究旨在更好地阐明其网络结果，可以帮助发现新的更为有效的抗癌策略。©2023. 作者

NRF2 is a transcription factor that plays a pivotal role in carcinogenesis, also through the interaction with several pro-survival pathways. NRF2 controls the transcription of detoxification enzymes and a variety of other molecules impinging in several key biological processes. This perspective will focus on the complex interplay of NRF2 with STAT3, another transcription factor often aberrantly activated in cancer and driving tumorigenesis as well as immune suppression. Both NRF2 and STAT3 can be regulated by ER stress/UPR activation and their cross-talk influences and is influenced by autophagy and cytokines, contributing to shape the microenvironment, and both control the execution of DDR, also by regulating the expression of HSPs. Given the importance of these transcription factors, more investigations aimed at better elucidating the outcome of their networking could help to discover new and more efficacious strategies to fight cancer.© 2023. The Author(s).