Bitterness in almonds (Prunus dulcis Miller D.A. Webb syn. Prunus amygdalus Batsch) is one of the most important and widely studied traits in this species. Almond bitterness is a monogenic trait, and the sweet taste allele is dominant over the bitter taste allele (Heppner, 1923, 1926; Dicenta and García, 1993; Dicenta et al., 2007). The gene responsible for bitterness in almonds is denoted Sweet kernel (Sk), and it is located in linkage group five, out of the eight that almond has (Sánchez-Pérez et al., 2007; 2010; Joobeur et al., 1998; Bliss et al., 2002). Commercial sweet genotypes can be homozygous (SkSk) or heterozygous (Sksk) for this trait, while slightly bitter genotypes are always heterozygous (Sksk), and bitter genotypes are homozygous recessive (sksk) (Grasselly et al., 1980; Vargas et al., 2001). The bitter trait is maternally controlled (Heppner, 1923; Dicenta and García, 1993; Kester and Gradziel, 1996; Socias, 1998; Sánchez-Pérez et al., 2010). As a result, all the fruits of an almond will be sweet, slightly bitter or bitter, and the influence of both progenitors will be seen in the next generation (Kester et al., 1975; Dicenta et al., 2000; Arrázola et al., 2012). Cyanogenic glucosides (CNGLcs) are β-glucosides of α-hydroxinitriles (Conn, 2007; Zheng and Poulton, 1995; Morant et al., 2008). These compounds are present in more than 3000 plant species (Bak et al., 2006a; Sánchez-Pérez et al., 2008; Gleadow and Møller, 2014) like sorghum, cassava and Rosaceous stone fruits. Their main function is to defend plants against pathogens and predators (Bak et al., 2006b; Zagrobelny et al., 2008). There are two cyanogenic glucosides present in almonds: prunasin (mono-glucoside of R-mandelonitrile) and amygdalin [di-glucoside of R-mandelonitrile with a β-(۱,۶) bond] (Conn, 2007; Sánchez-Pérez et al., 2008; McCarty et al., 1952; Frehner et al., 1990; Møller and Seigler, 1991; Swain et al., 1992a; Poulton and Ping Li, 1994; Dicenta et al., 2002; Franks et al., 2008). These two compounds are de novo synthesized in the almond seed (Sánchez-Pérez et al., 2008), and the amygdalin content is significantly higher in mature bitter almond seeds than in slightly bitter or sweet seeds (between 200 and 1000-fold higher, respectively). On the other hand, there is no clear relationship between the prunasin levels in the vegetative parts of the plant and the bitterness of the fruit (Dicenta et al., 2002). The almond fruit consists of maternal tissues (endocarp, mesocarp, tegument – also called the seed coat – and nucellus) and parental tissues endosperm (2n (mother) + n (father)) and cotyledon (n (mother) + n (father)). The first difference between sweet and bitter almonds can be found in the tegument, as prunasin only accumulates in the bitte teguments throughout seed development (Sánchez-Pérez et al., 2008). Fig. 1 describes the metabolism of prunasin and amygdalin, which can be divided into the following three parts: biosynthesis, bioactivation and detoxification.