Part of this variability is due to the residual activity of the p67phox protein as observed in patients with an Ala202Val substitution (Koker et al., 2013; Roos et al., 2014) or in patients with a splice variant that deletes exons 11 and 12 (Roesler et al., 2012), all of which have a less severe form of CGD with a delayed onset compared with p67phox null mutations (Table 2). This evidence concerns the gene NCF2 and chronic granulomatous disease.