Finally, monocytes from patients with a chronic granulomatous disease (CGD), which are constitutively defective in NOX2 due to mutations in one of the members of the NOX2 complex [27], demonstrated a similar defect in CSF-1-induced monocyte differentiation (Figure 4B–D), even though FAM-DEVD-FMK activity was similar to that measured in healthy controls, suggesting normal activation of caspases (Figure 4E). This evidence concerns the gene CYBB and chronic granulomatous disease.