Interestingly, in addition to the shared phenotypes (between PRLTS3 patients and CLPP−/− mice), PRLTS3 patients also exhibit some major neurological impairments such as epilepsy, microcephaly or learning difficulties, which suggests that some of the pathogenic mutations in CLPP might trigger a toxic gain-of-function in the mitochondrion. The gene discussed is CLPP; the disease is microcephaly.