The StAR protein was first identified, characterized and named by Dr. Douglas Stocco at Texas Tech University Health Sciences Center in 1994.  The role of this protein in lipoid CAH was confirmed the following year in collaboration with Dr. Walter Miller at the University of California, San Francisco .  All of this work follows the initial observations of the appearance of this protein and its phosphorylated form coincident with factors that caused steroid production by Dr. Nanette Orme-Johnson while at Tufts University . 
A number of investigators have reported on a rather rare syndrome of excess aromatase activity. In boys, it can lead to gynecomastia , and in girls to precocious puberty and gigantomastia . In both sexes, early epiphyseal closure leads to short stature. This condition is due to mutations in the CYP19A1 gene which encodes aromatase.  It is inherited in an autosomal dominant fashion.  It has been suggested that the pharaoh Akhenaten and other members of his family may have suffered from this disorder,  but more recent genetic tests suggest otherwise.  It is one of the causes of familial precocious puberty—a condition first described in 1937. 
A supportive single-blind , randomized clinical trial comparing high-dose, long-duration treatment (150 U/m 2 once daily for 3 weeks, n=30) of . Acthar Gel with low-dose, short-duration treatment (20 U once daily for 2 weeks, n=29) for the treatment of infantile spasms was also evaluated in infants and children less than 2 years of age. Nonresponders (defined as in the previously described study) in the low-dose group received a dose escalation at 2 weeks to 30 U once daily. Nominal statistical superiority of the high dose treatment, as compared to the low dose treatment, was observed for cessation of spasms but not for the resolution of hypsarrhythmia.