As the leading cause of deaths of infants of one month to one year of age, the exact etiology of Sudden Infant Death Syndrome (SIDS) remains uncertain. The initial emphasis on environmental factors such as infant sleeping position and second-hand smoke as the primary cause of SIDS has been replaced by a new focus on the low levels of adult hemoglobin in infants as a biological precursor to this fatal occurrence. Adult hemoglobin is a tetramer protein molecule in red blood cells whose specific structural conformation enables it to carry oxygen from the lungs and release it to the rest of the body. With an altered structure, fetal hemoglobin has an increased affinity for oxygen, facilitating the maternal transfer of oxygen in utero, but decreasing its ability to relinquish oxygen to tissues after birth. Therefore, delayed transition between fetal and adult hemoglobin can hinder the perfusion of oxygen in infants, leading to possible respiratory depression or an increased reliance on passive immunity, conditions that have been shown to increase infant susceptibility to SIDS. Research continues to study the differences in protein structure between each of these molecules as it relates to gene expression, but in the meantime, analysis of fetal hemoglobin levels remains a promising tool in the diagnosis of SIS.