Four major factors have been identified as playing complex interactive roles in pediatric obstructive sleep apnea syndrome (OSAS), namely craniofacial and anatomical factors, lymphoid tissue growth contributions, upper airway inflammation, and neuromuscular reflexes. In a series of studies, the gene encoding for apolipoprotein E (ApoE) was examined as potentially associated with the risk for OSAS. Oxidative stress appears to play a fundamental role in the pathophysiology of end-organ injury in the context of OSAS. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is an important gene that has been studied primarily in the context of the phagocyte oxidative burst. Fatty acid binding proteins (FABP) are a relatively large group of related molecules that serve as intracellular chaperones for lipid moieties, coordinate cellular lipid responses, and thereby play a critical role in metabolic and inflammatory pathways. In summary, phenotype-genotype interactions are clearly apparent in the context of pediatric OSAS.