The article discusses the role of signal transducer and activator of transcription (STAT) proteins, particularly STAT3, in cancer inflammation and immunity. STAT3 plays a central role in regulating cytokine-dependent inflammation and immunity, which can either promote or inhibit cancer. Persistent activation of STAT3 increases tumor cell proliferation, survival, and invasion while suppressing anti-tumor immunity. STAT3 also mediates tumor-promoting inflammation by promoting pro-oncogenic inflammatory pathways, such as the nuclear factor-κB (NF-κB) and interleukin-6 (IL-6)–GP130–Janus kinase (JAK) pathways, and by opposing STAT1- and NF-κB-mediated T helper 1 (Th1) anti-tumor immune responses. STAT3 is a promising target for cancer therapy, as it can be used to redirect inflammation towards anti-tumor immunity. The article highlights the importance of STAT3 in both the extrinsic and intrinsic pathways of cancer inflammation and its role in mediating inflammation-induced carcinogenesis. Additionally, it discusses the interaction between STAT3 and NF-κB, which are both crucial for pro-carcinogenic inflammation but also involved in anti-tumor immune responses. The article concludes by emphasizing the potential of targeting STAT3 as a therapeutic approach to convert cancer-promoting inflammation into anti-tumor immunity.The article discusses the role of signal transducer and activator of transcription (STAT) proteins, particularly STAT3, in cancer inflammation and immunity. STAT3 plays a central role in regulating cytokine-dependent inflammation and immunity, which can either promote or inhibit cancer. Persistent activation of STAT3 increases tumor cell proliferation, survival, and invasion while suppressing anti-tumor immunity. STAT3 also mediates tumor-promoting inflammation by promoting pro-oncogenic inflammatory pathways, such as the nuclear factor-κB (NF-κB) and interleukin-6 (IL-6)–GP130–Janus kinase (JAK) pathways, and by opposing STAT1- and NF-κB-mediated T helper 1 (Th1) anti-tumor immune responses. STAT3 is a promising target for cancer therapy, as it can be used to redirect inflammation towards anti-tumor immunity. The article highlights the importance of STAT3 in both the extrinsic and intrinsic pathways of cancer inflammation and its role in mediating inflammation-induced carcinogenesis. Additionally, it discusses the interaction between STAT3 and NF-κB, which are both crucial for pro-carcinogenic inflammation but also involved in anti-tumor immune responses. The article concludes by emphasizing the potential of targeting STAT3 as a therapeutic approach to convert cancer-promoting inflammation into anti-tumor immunity.