It is noteworthy that within our cohort, 26 patients with additional infections (Table 1) carried damaging variants in CLEC7A, PLCG2, or DUOX1/DUOXA1, compared with 6 of 27 patients without additional serious infections (Table 3) (n = 26 of 40 vs. 6 of 27; P = 0.001). The gene discussed is CLEC7A; the disease is infection.