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Single nucleotide polymorphisms (SNPs) in the gene encoding kinesin family member 3A,  KIF3A , have been associated with atopic dermatitis (AD), a chronic inflammatory skin disorder. We find that  KIF3A  SNP rs11740584 and rs2299007 risk alleles create cytosine-phosphate-guanine sites, which are highly methylated and result in lower  KIF3A  expression, and this methylation is associated with increased transepidermal water loss (TEWL) in risk allele carriers.  Kif3a   K14 ∆ / ∆  mice have increased TEWL, disrupted junctional proteins, and increased susceptibility to develop AD. Thus,  KIF3A  is required for skin barrier homeostasis whereby decreased  KIF3A  skin expression causes disrupted skin barrier function and promotes development of AD.

Disease-associated KIF3A variants alter gene methylation and expression impacting skin barrier and atopic dermatitis risk