It is tempting to speculate that parvalbumin+ protein expression may be reduced in an activity‐dependent manner due to metabolic failure arising from extensive OXPHOS deficiencies and reduced excitatory input from pyramidal neurons, due to severe pyramidal neuron loss in Alpers' syndrome [36, 37], whereas the majority of patient calretinin+ interneurons showed normal or increased levels of calretinin+ protein suggesting preserved activity of calretinin+ interneurons and intact calcium buffering capacity, which may partly underlie the increased resilience of these interneurons. The gene discussed is PVALB; the disease is Alpers syndrome.