Traumatic brain injury (TBI) is a major public health problem with potentially debilitating consequences for the individual. Hypopituitarism after TBI has received increasing attention over the past decade; development of the condition as a consequence of TBI was previously hardly mentioned in textbooks on the subject. Hypopituitarism has been reported in more than 25% of patients with TBI and is now thought to be one of the most important causes of treatable morbidity in TBI survivors. However, most clinicians dealing with neuroendocrine diseases and TBI generally do not see such a high incidence of hypopituitarism. This disproportion is not clearly explained, but recent data indicate that diagnostic testing, which is designed for high-risk populations and not for a cohort of patients with, for example, de novo isolated growth hormone deficiency (the predominant finding in TBI), might have overestimated the true risk and disease burden of hypopituitarism. In this Opinion article, we discuss current recommendations for post-traumatic hypopituitarism in light of recent evidence.