Maiti et al. studied placentae from three groups: term (39 weeks), late term (>41 weeks), and idiopathic stillbirths; they found increased aldehyde oxidase 1 expression (a mediator of placental ageing), DNA/RNA and lipid oxidation, lysosomes situated perinuclearly and basally as opposed to apically when localised with lysosome-associated membrane protein 2 (LAMP2), and bigger autophagosomes suggestive of inhibition of function in later-term placentae [12]. The gene discussed is LAMP2; the disease is Stillbirth.