In addition, one limitation of our study is that it remains unknown whether the systemic inflammation observed in ROSAH patients is due to a direct action of ALPK1 in myeloid cells or in other cell types (e.g., in the eye or in the sweat glands), in which the IFN-γ-mediated regulation of TIFA may be less important. This evidence concerns the gene ALPK1 and retinal dystrophy, optic nerve edema, splenomegaly, anhidrosis, and migraine headache syndrome.