Further studies on the Bcs1lp.S78G mice, displaying in some tissues by far the most staggering “cancer-like” MYC upregulation of all mitochondrial disease models, could shed light on the role OXPHOS dysfunction in carcinogenesis if crossed with mice carrying mutant alleles of major tumor suppressor pathways such as p53 or APC (Adenomatosis Polyposis Coli tumor suppressor). Here, MYC is linked to inborn mitochondrial metabolism disorder.