In general, perinatal and infantile subtypes represent severe forms of HPP, while childhood, adult, odonto, and prenatal benign subtypes constitute mild phenotypes.[4] HPP is caused by loss-of-function mutations in the ALPL gene encoding the Tissue Nonspecific Alkaline Phosphatase (TNSALP).[5] TNSALP is a membrane-bound metalloenzyme, whose activity is reduced by various mutations in the ALPL gene, leading to the increased inorganic pyrophosphate, which in turn causes different HPP phenotypes [6]. This evidence concerns the gene ALPL and hypophosphatasia.