Normophosphataemic familial tumoral calcinosis, charac‐terized by ectopic mineralization of skin, is caused by mutations in the SAMD9 gene located in human chromosome 7q21, next to a paralogous gene, SAMD9‐like (SAMD9L). The mouse does not have a SAMD9 orthologue, Samd9, because it has been deleted during evolution owing to genomic rearrangements. It has been suggested that the mouse Samd9l gene serves as a functional paralogue of human SAMD9. In this study, we examined Samd9l knockout mice with respect to ectopic mineralization. We also crossed these mice with Abcc6^tm1JfK mice, a model system to study pseudoxanthoma elasticum, to see whether the absence of the Samd9l gene modifies the mineralization process. Necropsy analysis of Samd9l^tm1Homy mice revealed no evidence of ectopic mineralization, and deletion of the Samd9l gene in mice failed to modify the mineralization process on the Abcc6^tm1JfK background. Collectively, the results suggest that mouse Samd9l is not a functional paralogue of human SAMD9.