In this study, we present the case of a young child with recurrent and severe viral infections who was found to have a heterozygous variant in FBN2 as well as homozygous variants in both IFNAR1 and DOCK8. While the FBN2 variant explained congenital contractual arachnodactyly, homozygous variants in DOCK8 and IFNAR1 potentially underpinned the infectious complications in this case, thereby necessitating further investigation. The gene discussed is DOCK8; the disease is congenital contractural arachnodactyly.