Given that (i) several mitochondrial proteins with clear roles in intermediary metabolism have been shown to be S-palmitoylated in a variety of biological systems10–12 and (ii) alopecia—as observed in our3 and another12 mouse model of Zdhhc13 deficiency—has been linked to mitochondrial dysfunction13,14, we hypothesized that Zdhhc13 loss-of-function would result in deficits in bioenergetics, not necessarily limited to skin, but to other highly aerobic organs such as brain resulting in behavioral deficits associated with energy distress and altered metabolism of neurotransmitters. The gene discussed is ZDHHC13; the disease is alopecia.