This study investigates the role of exosome-derived circular RNA (circRNA) circATP8A1 in gastric cancer progression. CircATP8A1, a novel circRNA not previously reported, is highly expressed in gastric cancer tissues and plasma exosomes. Increased circATP8A1 levels are associated with advanced TNM stage and poor prognosis in gastric cancer patients. knockdown of circATP8A1 significantly inhibits gastric cancer proliferation, invasion, and migration both in vitro and in vivo. Functionally, exosome circATP8A1 induces M2 polarization of macrophages through the STAT6 pathway, rather than the STAT3 pathway. Mechanistically, circATP8A1 activates the STAT6 pathway by competitively binding to miR-1-3p, as confirmed by various experimental methods. The reversal of circATP8A1-induced STAT6 pathway activation and macrophage polarization is observed upon blocking miR-1-3p. Macrophages treated with exosomes from gastric cancer cells overexpressing circATP8A1 promote gastric cancer migration, while knockdown of circATP8A1 reverses these effects in vivo. In conclusion, exosome-derived circATP8A1 induces macrophage M2 polarization via the circATP8A1/miR-1-3p/STAT6 axis, promoting gastric cancer progression. These findings highlight circATP8A1 as a potential prognostic biomarker and therapeutic target in gastric cancer.This study investigates the role of exosome-derived circular RNA (circRNA) circATP8A1 in gastric cancer progression. CircATP8A1, a novel circRNA not previously reported, is highly expressed in gastric cancer tissues and plasma exosomes. Increased circATP8A1 levels are associated with advanced TNM stage and poor prognosis in gastric cancer patients. knockdown of circATP8A1 significantly inhibits gastric cancer proliferation, invasion, and migration both in vitro and in vivo. Functionally, exosome circATP8A1 induces M2 polarization of macrophages through the STAT6 pathway, rather than the STAT3 pathway. Mechanistically, circATP8A1 activates the STAT6 pathway by competitively binding to miR-1-3p, as confirmed by various experimental methods. The reversal of circATP8A1-induced STAT6 pathway activation and macrophage polarization is observed upon blocking miR-1-3p. Macrophages treated with exosomes from gastric cancer cells overexpressing circATP8A1 promote gastric cancer migration, while knockdown of circATP8A1 reverses these effects in vivo. In conclusion, exosome-derived circATP8A1 induces macrophage M2 polarization via the circATP8A1/miR-1-3p/STAT6 axis, promoting gastric cancer progression. These findings highlight circATP8A1 as a potential prognostic biomarker and therapeutic target in gastric cancer.