This study showed an abundant HMBS protein expression in hepatocytes of Hmbs-deficient mice and rapidly normalising urine porphyrin precursor excretion in ongoing attacks, and in a chemically induced acute porphyria rabbit model, thus providing proof-of-concept for systemic human HMBS mRNA as a potential therapy for AIP [120]. The gene discussed is HMBS; the disease is hepatic porphyria.