Other sites include L196P, R258S, P197/F198L, R202I, Q207E, G325A, G328W/ G328E/G328R, G356D, R375P.[15–18] Some patients with atypical mutations can have more severe presentations.[2] The genetic breakthrough of inducing abnormal activation of bone morphogenetic proteins as the cause of FOP lesions established a critical milestone in our understanding FOP, and open the doors to find a highly conserved therapeutic target for the disease.[11] The confirmatory genetic mutation testing of ACVR1/ALK2 is crucial to confirm a diagnosis of FOP before the appearance of heterotopic ossifications. This evidence concerns the gene ACVR1 and fibrodysplasia ossificans progressiva.