Non-alcoholic fatty liver disease (NAFLD) is a prevalent liver disorder characterized by excessive fat accumulation in the liver, often associated with metabolic syndrome. Inflammatory cytokines, particularly interleukins (ILs), play a crucial role in the pathogenesis of NAFLD. ILs, initially thought to be produced only by leukocytes, are now known to be produced by various cells throughout the body and exhibit both pro-inflammatory and anti-inflammatory properties. The specific roles of different ILs in NAFLD vary, and ongoing research aims to understand these mechanisms. Environmental factors and genetics can influence the onset and progression of NAFLD, and while clinical studies on the therapeutic potential of IL-1 inhibitors are limited, preclinical studies show promising results. The pathophysiology of NAFLD is complex, involving multiple factors such as oxidative stress, inflammation, insulin resistance, and dyslipidemia. Inflammation, triggered by the accumulation of fat in the liver, can lead to more severe forms of NAFLD, such as non-alcoholic steatohepatitis (NASH). Pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α are key contributors to the development and progression of NAFLD. Recent studies have highlighted the role of the inflammasome, particularly the NLRP3 inflammasome, in the inflammatory response and fibrosis progression in NAFLD. Interleukin-1 (IL-1) is a potent inflammatory cytokine produced by macrophages and other cells. IL-1α and IL-1β are involved in the late stages of inflammation and are linked to NASH progression. IL-1β inhibition has shown positive effects on cardiac diastolic function but did not ameliorate NASH features. IL-18, another IL-1 family member, is also implicated in liver injury in NAFLD. Other ILs, such as IL-2, IL-4, IL-5, IL-6, and IL-7, have been studied for their roles in NAFLD. IL-2 is involved in T-cell proliferation and antibody production, while IL-4 is a prototypic immunoregulatory cytokine. IL-5 is involved in eosinophil function and asthma, and IL-6 plays a crucial role in host defense and acute phase responses. IL-7 is important for lymphoid cell development and protection from apoptosis. Recent studies have explored the potential of IL-1 inhibitors as therapeutic options for NAFLD, although more research is needed to fully understand their efficacy. The complex interplay between pro-inflammatory and anti-inflammatory cytokines in NAFLD highlights the need for targeted therapeutic interventions to improve clinical outcomes.Non-alcoholic fatty liver disease (NAFLD) is a prevalent liver disorder characterized by excessive fat accumulation in the liver, often associated with metabolic syndrome. Inflammatory cytokines, particularly interleukins (ILs), play a crucial role in the pathogenesis of NAFLD. ILs, initially thought to be produced only by leukocytes, are now known to be produced by various cells throughout the body and exhibit both pro-inflammatory and anti-inflammatory properties. The specific roles of different ILs in NAFLD vary, and ongoing research aims to understand these mechanisms. Environmental factors and genetics can influence the onset and progression of NAFLD, and while clinical studies on the therapeutic potential of IL-1 inhibitors are limited, preclinical studies show promising results. The pathophysiology of NAFLD is complex, involving multiple factors such as oxidative stress, inflammation, insulin resistance, and dyslipidemia. Inflammation, triggered by the accumulation of fat in the liver, can lead to more severe forms of NAFLD, such as non-alcoholic steatohepatitis (NASH). Pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α are key contributors to the development and progression of NAFLD. Recent studies have highlighted the role of the inflammasome, particularly the NLRP3 inflammasome, in the inflammatory response and fibrosis progression in NAFLD. Interleukin-1 (IL-1) is a potent inflammatory cytokine produced by macrophages and other cells. IL-1α and IL-1β are involved in the late stages of inflammation and are linked to NASH progression. IL-1β inhibition has shown positive effects on cardiac diastolic function but did not ameliorate NASH features. IL-18, another IL-1 family member, is also implicated in liver injury in NAFLD. Other ILs, such as IL-2, IL-4, IL-5, IL-6, and IL-7, have been studied for their roles in NAFLD. IL-2 is involved in T-cell proliferation and antibody production, while IL-4 is a prototypic immunoregulatory cytokine. IL-5 is involved in eosinophil function and asthma, and IL-6 plays a crucial role in host defense and acute phase responses. IL-7 is important for lymphoid cell development and protection from apoptosis. Recent studies have explored the potential of IL-1 inhibitors as therapeutic options for NAFLD, although more research is needed to fully understand their efficacy. The complex interplay between pro-inflammatory and anti-inflammatory cytokines in NAFLD highlights the need for targeted therapeutic interventions to improve clinical outcomes.