Premature ovarian failure (POF) appears to be a complex disease entity with several underlying etiopathogenic contributions including the possibility of multiple distinctly different autoimmune mechanisms, in which inflammatory autoimmunity targeted to ovarianspecific germline antigens (e.g., zona pellucida proteins or Mater) or differentiation/regulatory factors (e.g. inhibin-alpha) were regarded as one of the most crucial factors. Platelet-activating factor (PAF) and PAF class oxidized phospholipids stimulate the occurrence and development of inflammation and atherosclerosis. PAF acetylhydrolase (PAF-AH) can hydrolyze PAF and PAF class oxidized phospholipids and eventually prevent the body from the damage of these inflammatory mediators. These findings indicate a potential relationship between PAF-AH and POF thus have major implications for the future health of women who suffer with premature ovarian failure.