UNC13D and hemophagocytic syndrome: Having said that, in the current study, the previously reported case of homozygous p.Arg414Cys pathogenicity (8), the invariable conservation of p.Arg414 and p.Ala918, the extreme rarity of both mutations, the uniform in silico prediction of pathogenicity of the mutations, and the impaired degranulation which is corrected posttransplant (Figure 2), all strongly suggests that FHL was due to the bi-allelic mutations in UNC13D outlined above.