The PARL proteolytic and signaling cascade has diverse downstream targets in addition to PGAM5, including phosphatase and tensin homolog–induced kinase 1, BCL-xL, FUNDC1, and others, with sundry effects on mitochondrial and cellular metabolism and survival, and thus represents a wide area for future study in tafazzin deficiency (47, 48). The gene discussed is FUNDC1; the disease is hyperinsulinemic hypoglycemia, familial, 4.