Because in the experiment described above, IL17A‐deficient CD3+ T cells nevertheless retained their ability to infiltrate into degenerating HFs, thus maintaining a strong correlation with radiodermatitis and alopecia, we instead sought to determine the effect of disrupting the CCL20/CCR6 chemokine signaling that mediates migration of IL‐17‐producing cells (Yamazaki et al, 2008) on IRIAD. The gene discussed is IL17A; the disease is alopecia.