Atrial fibrillation (AF) is the most common sustained arrhythmia. Clonal hematopoiesis of indeterminate potential, characterized by the clonal expansion of hematopoietic stem cells owing to acquired mutations without hematologic malignancies, has emerged as a potential risk factor for AF. This narrative review summarizes the shared risk factors between clonal hematopoiesis of indeterminate potential and AF, including age, lifestyle behaviors, and cardiometabolic conditions. It then explores the underlying mechanisms including inflammation, atrial fibrosis, and abnormal red cell distribution width. Among these, inflammation is a central driver that promotes abnormal calcium handling, which further accelerates atrial remodeling. For specific mutations, TET2 mutations correlate strongest with AF, and other mutations in genes, such as ASXL1, JAK2, TP53, and PPM1D, and spliceosomes, may also modulate AF susceptibility, although their precise roles require further investigation.