Damaging variants in SLC39A14 and ANO5, both encoding transporters with a prominent function in osteoblasts, are responsible for HBM conditions hyperostosis cranialis interna (OMIM 144755)(14) and gnathodiaphyseal dysplasia (OMIM 166260), respectively.(46) Similarly for osteoclasts, mutations in SLC29A3 and SLC4A2 encoding respective nucleoside and anion transporters cause dysosteosclerosis (OMIM 224300)(45) and recessive osteopetrosis, Ikegawa type (OMIM n.a.)(Table S1).(47). Here, SLC29A3 is linked to dysosteosclerosis.