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Although the same gene, CYP21A2, is involved in both the severe and mild forms, genetic mutations typically associated with non-classic CAH result in substantially less impairment of hydroxylase activity. Thus, patients with non-classic CAH do not have cortisol deficiency but instead may have manifestations of hyperandrogenism, later in childhood or in early adulthood. Treatment of the mild or non-classic form is targeted at controlling excess androgen symptoms and may or may not involve glucocorticoid therapy. Longer-acting glucocorticoids have typically been avoided in children due to their potential for growth suppression No consensus exists for glucocorticoid dosing in adults.