The protective role of fetal haemoglobin (HbF) was discovered in the 1940s, when Dr. Janet Watson suggested a link between HbF levels and the presence of disease symptoms in 1948. She observed that higher HbF levels in newborns kept them asymptomatic. Humans possess predominantly HbF in their fetal life but within 12 weeks after birth the production of HbF production is shut off and replaced by the production of adult haemoglobin HbA. It is now known that in some sickle cell patients this switch does not occur as efficiently, resulting in higher than normal HbF levels. These differences in HbF levels mark the differences between symptom manifestation where patients with higher HbF levels have a milder form of the disease.