Abstract: Recently, it has been reported that a genetic background may play a role in plasma cytokine levels induced by several conditions ranging from psoriasis, eclempsia, sepsis and post-operative complications. Among these, is the gene for tumor necrosis factor-alpha (TNF- ), a cytokine known to exert a range of inflammatory and immunomodulatory activities important in the host defence mechanisms. Indeed, TNF- has been implicated in the pathogenesis of several conditions including cardiovascular, eclempsia, psoriasis, rheumatoid arthritis (RA), septic shock and myocardial dysfunction. Currently, the focus is on the mechanisms that modulate TNF- production, which in turn impact on the disease-mediated inflammatory process. Various polymorphisms have been identified within and around the TNF- -encoding gene located within the major histocompatibility complex (MHC). In the promoter region relative to the transcription start site, there are several single nucleotide polymorphisms (SNPs), at positions -1031 (T C), -863 (C A), -857 (C A), -851 (C T), -419 (G C), -376 (G A), -308 (G A), -238 (G A), -162 (G A) and -49 (G A). However, those at positions -419, -163, -49, are rare in Caucasians. This review has highlighted the conflicting results among various publications on the associations between -308 TNF SNPs and TNF production. In addition, we have specifically reviewed the association between genotype distribution and allele frequencies of TNF NcoI gene polymorphism at the -308 positions and the pathophysiologic changes induced by coronary heart disease.