Transwell migration was particularly increased in the presence of osteopontin (OPN), a highly phosphorylated ECM protein previously suggested to be a physiological substrate for TRAP [10], and involved in the progression of TRAP-related pathologies such as the immuno-osseous disorder Spondyloenchondrodysplasia [9, 62]. The gene discussed is SPP1; the disease is Spondyloenchondrodysplasia with immune dysregulation.