Throughout the last 20 years, the concept of auto-inflammation is developed, culminating with the finding of how gene mutations of Mediterranean Fever (MEFV) seemed to be causally linked to Familial Mediterranean fever (FMF). The autoinflammatory illnesses presently constitute a wide variety of disorders that have mutual signs of frequent fever, the incidence of hyper-reactive immune cells of hereditary origin, and indicators of inflammation that may occur systemically or specific to an organ with no autoimmunity specific infection. The key causes of the unregulated inflammation are the myeloid innate immune cells which mainly induced production of excessive inflammatory cytokines as IL-1β and IL-18. Deficiencies through various signalling mechanisms regulating innate immune response, especially a single and even multiple inflammasomes hyperreactivity, remain the essence of pathological autoinflammatory phenotype. While FMF would be a monogenic autoinflammatory syndrome, it is genetically complicated and affected by environmental influences. Lately, epigenetic dysregulation has appeared to be a further cause of pathogenesis.Throughout this survey, we are addressing the epigenetic involvement pathways within (FMF).