No human Mendelian genetic disease has yet been attributed to loss-of-function mutations in BGLAP, in the Online Mendelian Inheritance in Man or MatchMaker exchange databases ([28, 29] https://omim.org and https://www.matchmakerexchange.org, each accessed on December 5, 2019), and there seems to be tolerance for heterozygous loss-of-function mutations at the population level (pLI = 0) [30] in the gnomAD database [https://gnomad.broadinstitute.org]. This evidence concerns the gene BGLAP and hereditary disease.