NOCT (nocturnin) is a circadian-regulated phosphatase that converts NADP(+) to NAD(+) and NADPH to NADH, with a slight preference for NADPH 1. Beyond its phosphatase activity, NOCT represses translation and promotes degradation of target mRNAs 2, exerting rhythmic post-transcriptional control over metabolic genes including those regulating glucose/insulin sensitivity and lipid metabolism 3. NOCT exhibits tissue and cell-specific differential processing, localizing to the cytoplasm or mitochondria to regulate both mRNA and NAD(H)/NADP(H) cofactor levels 2. The enzyme promotes adipogenesis while inhibiting osteoblastogenesis through PPARγ-dependent mechanisms 4. Structurally, NOCT shares similarity to deadenylase family members but possesses unique active-site properties and lacks poly-A RNA deadenylase activity 5. Clinically, NOCT dysregulation is implicated in pulmonary hypertension pathogenesis, where ADAR1-mediated RNA editing normally suppresses NOCT expression; loss of this regulation increases NOCT levels, triggering endothelial apoptosis and vascular remodeling 6. NOCT also plays a critical role in metabolic dysfunction-associated steatotic liver disease, with circadian disruption causing phase shifts in its expression 3. NAD(H)/NADP(H) homeostasis dysregulation through impaired NOCT function is associated with cancer and metabolic disorders 7.