The internal pathophysiology of TrPs suggests localized tissue hypoxia, increased acute inflammatory cascade (bradykinin, substance P, interleukin-1), and lowered pH (acidosis).1The first hypothesis, related to TrPs etiology, describes a mitochondrial dysfunction in the development of TrPs.3Recently, Fisheret al. analyzed a muscle biopsy in active TrPs to evaluate mitochondrial function. This evidence concerns the gene KNG1 and trichorhinophalangeal syndrome.