Despite the ability of DECTIN-1 to activate NADPH oxidase activity in both DUOX1/DUOXA1 and NOX2/gp91phox systems, patients with chronic granulomatous disease due to defects in the NOX2 complex do not have increased risk of infection from Coccidioides (53), and gp91phox mice have normal resistance to intranasal Coccidioides infection (54, 55). This evidence concerns the gene CLEC7A and coccidioidomycosis.