In WHIM (warts, hypogammaglobulinemia, infections, and myelokathexis) syndrome, heterozygous mutations in the C‐terminus of CXCR4 result in a similar truncation to the one we describe here, which ablates the binding of GRK3 and GRK6, leading to defective CXCR4 phosphorylation and internalization and enhanced chemotactic responses to ligand.39 This evidence concerns the gene CXCR4 and infection.