Fibrodysplasia ossificans progressiva (FOP) is a rare genetic disorder causing progressive heterotopic ossification (HO) of muscles, tendons, and ligaments.1, 2 The activating R206H mutation of the bone morphogenetic protein (BMP) type 1 receptor ACVR1 accounts for most of the classical FOP cases.3, 4 From early childhood onward, the disease becomes gradually worse owing to active periods (flare‐ups), which may be spontaneous or induced by trauma or surgery.5 The underlying mechanism of flare‐ups is complex and not well understood, no validated biomarkers of flare‐ups exist. This evidence concerns the gene ACVR1 and fibrodysplasia ossificans progressiva.