This review discusses the epidemiology and genetics of rheumatoid arthritis (RA), highlighting the interplay between genetic and environmental factors in its development. RA prevalence is relatively stable at 0.5–1.0% in many populations, but is higher in certain groups, such as the Pima and Chippewa Indians (5.3% and 6.8%, respectively), and lower in populations from China and Japan. These variations suggest a genetic component in RA risk. The HLA DRB1 alleles, particularly DRB1*0404, are the strongest genetic risk factors, though they explain only about 50% of the genetic effect. Other non-MHC genes, such as those involved in cytokine production, have also been linked to RA. Environmental factors, including hormonal influences and pregnancy, play a role in RA. Female sex hormones may offer protection, while the postpartum period, especially after the first pregnancy, is a high-risk time for RA onset. Breastfeeding after the first pregnancy is associated with increased risk. Smoking is also linked to RA, with data suggesting an increased risk. Infection may act as a trigger, though evidence is inconclusive. Other environmental factors, such as diet and obesity, have been studied, but their roles are less clear. The review emphasizes the complex interaction between genetic and environmental factors in RA. Twin studies show a higher concordance in monozygotic twins, indicating a genetic contribution, but the exact role remains unclear. Future research aims to identify new genetic factors through molecular biology techniques and to better understand the environmental influences on RA. Overall, the study underscores the importance of both genetic and environmental factors in RA development and highlights the need for further research to clarify their interactions.This review discusses the epidemiology and genetics of rheumatoid arthritis (RA), highlighting the interplay between genetic and environmental factors in its development. RA prevalence is relatively stable at 0.5–1.0% in many populations, but is higher in certain groups, such as the Pima and Chippewa Indians (5.3% and 6.8%, respectively), and lower in populations from China and Japan. These variations suggest a genetic component in RA risk. The HLA DRB1 alleles, particularly DRB1*0404, are the strongest genetic risk factors, though they explain only about 50% of the genetic effect. Other non-MHC genes, such as those involved in cytokine production, have also been linked to RA. Environmental factors, including hormonal influences and pregnancy, play a role in RA. Female sex hormones may offer protection, while the postpartum period, especially after the first pregnancy, is a high-risk time for RA onset. Breastfeeding after the first pregnancy is associated with increased risk. Smoking is also linked to RA, with data suggesting an increased risk. Infection may act as a trigger, though evidence is inconclusive. Other environmental factors, such as diet and obesity, have been studied, but their roles are less clear. The review emphasizes the complex interaction between genetic and environmental factors in RA. Twin studies show a higher concordance in monozygotic twins, indicating a genetic contribution, but the exact role remains unclear. Future research aims to identify new genetic factors through molecular biology techniques and to better understand the environmental influences on RA. Overall, the study underscores the importance of both genetic and environmental factors in RA development and highlights the need for further research to clarify their interactions.