ACVR1 and fibrodysplasia ossificans progressiva: Indeed, the initial causal mechanisms that trigger NHOs are unique to this pathology, as they involve severe CNS trauma17,18 rather than other forms of trauma, such as body burns, or activating mutations of osteogenic genes, such as bone morphogenetic protein type I receptor ACVR1, in fibrodysplasia ossificans progressiva (FOP).17 Therefore, it is essential to uncover the mechanisms of NHO pathogenesis to identify potential therapeutic targets and treatments that will reduce NHO development and remove the need for very invasive and delicate surgical resections.17