An 11-y-old boy presented with complaints of multiple nodules over upper back and suboccipital region for last 2.5 y. There was associated gradual limitation of movement of neck, followed by right shoulder. The child had received 8 mo of antitubercular therapy and 3 mo of Albendazole after a presumptive diagnosis of tuberculosis and cysticercosis was made elsewhere. On examination, the child had nontender nodules with bony consistency over the back, suboccipital region, chest and abdominal wall. No definitive diagnosis could be made even after consultation with pediatrician and pediatric orthopedician. At open diagnostic biopsy, well formed flat bones in paraspinal muscles with globular swelling which felt like partially calcified cartilage were noticed. The histopathological examination revealed mature bone. Skeletal survey revealed shortened first metatarsal and proximal phalanges of bilateral great toe with hallux valgus (Fig. 1). There was linear ossification in the muscles of back extending from the base of the skull till the sacrum (S1 level). Corroboration of clinical and histopathological features suggested a diagnosis of FOP (Fibrodysplasia ossificans progressive). Audiometry revealed bilateral mild conductive hearing loss. Fibrodysplasia ossificans progressive (FOP) is a progressive, debilitating disease with a prevalence of 0.61 per million but with no described effective treatment [1]. FOP can be diagnosed on the basis of a diagnostic triad: congenital skeletal malformation of the great toes; progressive heterotopic ossification of skeletal muscles, tendons, ligaments, and fascia and progression of disease activity in characteristic anatomic patterns (dorsal to ventral, axial to appendicular, cranial to caudal, and proximal to distal) [2]. Nearly 90 % of FOP patients worldwide are misdiagnosed, and 67 % undergo dangerous and unnecessary diagnostic procedures that lead to permanent harm and lifelong disability in more than 50 % of all affected individuals [3]. Biopsy or excision is useless as the heterotopic bone in FOP is indistinguishable histologically frommature skeletal bone [4]. The genetic defect in FOP (phenotype MIM no 135100) involves mutation in the gene encoding activin receptor IA (gene MIM no 102576) located on chromosome 2q and makes it amenable to genetic testing [5]. Regular assessment of the patient’s functional status by a physiotherapist and occupation therapist is needed to ensure that functionality is maintained. Deep soft issue trauma, intramuscular Fig. 1 Clinical photograph of the foot showing shortened bilateral great toe with hallux valgus