**1. Introduction**

Rheumatoid arthritis (RA) is a chronic autoinflammatory disease affecting connective tissue, characterised by progressive joint damage and specific systemic disorders. To date, the number of patients with autoimmune arthritis is almost 1% of the world's population, establishing an urgent problem for healthcare systems worldwide. An evident feature of RA is clinical polymorphism, represented by a wide variability of symptoms, clinical forms, and progression rates. RA is considered to

be a multifactorial disease triggered by a genetic predisposition and environmental factors. Both clinical and genealogical studies have shown that the disease can accumulate in families. This relationship has been confirmed by modern molecular genetics. The opportunity to identify RA risk groups in different populations, as well as the possible prognostic value of some genetic variants for disease development, progression, and treatment, including a personalised antirheumatic therapy response, has promoted new studies of germline genetic variants in RA patients [1,2]. This review has two purposes. First, to summarise the data on the RA candidate genes in various populations and the increased disease risk associated with those alleles. Second, to describe how the genetic variants can be used in the selection of drugs such as methotrexate, interleukin-6 signalling pathway inhibitors or TNF (tumor necrosis factor) inhibitors for the treatment of RA. Papers in the PubMed and Scopus databases published in 2010–2020, as well as clinical recommendations and information materials from the American College of Rheumatology and the European League Against Rheumatism, were analysed to understand the current state in this field. A total of 125 sources were selected, of which 96 are mentioned in this review.
