Rosacea is a common inflammatory skin disease with a multifaceted pathophysiology, including environmental stressors and neurovascular and immune dysfunction affected by the presence of pathogens. The genetic component of this disorder is not well understood. However, a possible genetic origin in Northern European descendants, family inheritance, twin concordance, and genetic associations with autoimmune disorders attest the genetic predisposition to rosacea. Currently, one single-nucleotide polymorphism has been identified in association with rosacea and is intergenic between HLA-DRA and BTNL2. Additional associations with HLA alleles and immune-mediated disorders support the role of immune-regulating genes and innate and adaptive immunity in rosacea.