STAT3 plays a central role in cancer inflammation and immunity. It is involved in promoting tumour growth by enhancing pro-oncogenic inflammatory pathways, such as NF-κB and IL-6–JAK, while suppressing anti-tumour immunity. Persistent activation of STAT3 also mediates tumour-promoting inflammation. STAT3 interacts with NF-κB, contributing to constitutive NF-κB activation in cancer. Both proteins regulate oncogenic and inflammatory genes, and their persistent activation is crucial for inflammation and malignant progression. STAT3 is a promising target for cancer therapy as it can redirect inflammation to benefit cancer treatment. STAT3 and NF-κB are key regulators of inflammation and cancer. They are involved in both intrinsic and extrinsic pathways of cancer inflammation. STAT3 is crucial for pro-carcinogenic inflammation and suppresses anti-tumour immunity by antagonizing NF-κB- and STAT1-mediated expression of antitumour T helper 1 (T H1) cytokines. STAT3 also mediates T regulatory cell expansion and T H17 T cell development, which can promote tumour growth. A feedforward loop between tumour cells and immune cells in the tumour microenvironment is established through STAT3 signalling. STAT3 is involved in various cancers, including liver, gastric, and colorectal cancers, and is linked to inflammation-associated tumorigenesis. It is activated by genetic and environmental factors, including chemical carcinogens, infections, and stress. STAT3 is also involved in non-infectious carcinogenesis, such as UV-induced skin cancer and cigarette smoke-associated cancer. STAT3 is a major mediator of pro-carcinogenic inflammation and opposes NF-κB and STAT1-dependent immune responses that promote anti-tumour immunity. Targeting STAT3 for cancer therapy is a promising approach. Inhibitors of STAT3, including small molecules, oligonucleotides, and natural products, have been developed. These inhibitors can block tumour cell proliferation and survival, and convert tumour-promoting inflammation to anti-tumour immunity. Tyrosine kinase inhibitors, such as sorafenib and sunitinib, can indirectly inhibit STAT3 signalling and modulate the tumour immunological microenvironment. STAT3 is a central regulatory node on which many oncogenic and inflammatory pathways converge, making it a promising target for future cancer therapy.STAT3 plays a central role in cancer inflammation and immunity. It is involved in promoting tumour growth by enhancing pro-oncogenic inflammatory pathways, such as NF-κB and IL-6–JAK, while suppressing anti-tumour immunity. Persistent activation of STAT3 also mediates tumour-promoting inflammation. STAT3 interacts with NF-κB, contributing to constitutive NF-κB activation in cancer. Both proteins regulate oncogenic and inflammatory genes, and their persistent activation is crucial for inflammation and malignant progression. STAT3 is a promising target for cancer therapy as it can redirect inflammation to benefit cancer treatment. STAT3 and NF-κB are key regulators of inflammation and cancer. They are involved in both intrinsic and extrinsic pathways of cancer inflammation. STAT3 is crucial for pro-carcinogenic inflammation and suppresses anti-tumour immunity by antagonizing NF-κB- and STAT1-mediated expression of antitumour T helper 1 (T H1) cytokines. STAT3 also mediates T regulatory cell expansion and T H17 T cell development, which can promote tumour growth. A feedforward loop between tumour cells and immune cells in the tumour microenvironment is established through STAT3 signalling. STAT3 is involved in various cancers, including liver, gastric, and colorectal cancers, and is linked to inflammation-associated tumorigenesis. It is activated by genetic and environmental factors, including chemical carcinogens, infections, and stress. STAT3 is also involved in non-infectious carcinogenesis, such as UV-induced skin cancer and cigarette smoke-associated cancer. STAT3 is a major mediator of pro-carcinogenic inflammation and opposes NF-κB and STAT1-dependent immune responses that promote anti-tumour immunity. Targeting STAT3 for cancer therapy is a promising approach. Inhibitors of STAT3, including small molecules, oligonucleotides, and natural products, have been developed. These inhibitors can block tumour cell proliferation and survival, and convert tumour-promoting inflammation to anti-tumour immunity. Tyrosine kinase inhibitors, such as sorafenib and sunitinib, can indirectly inhibit STAT3 signalling and modulate the tumour immunological microenvironment. STAT3 is a central regulatory node on which many oncogenic and inflammatory pathways converge, making it a promising target for future cancer therapy.