NMRK1 (nicotinamide riboside kinase 1) catalyzes the phosphorylation of nicotinamide riboside (NR) and nicotinic acid riboside (NaR) to form nicotinamide mononucleotide (NMN) and nicotinic acid mononucleotide (NaMN), respectively, serving as a key enzyme in the NAD+ salvage pathway 1. The enzyme plays a critical role in maintaining hepatic NAD+ levels; NRK1 overexpression in mouse liver elevates NAD+ content, reduces hepatic steatosis, and improves glucose tolerance and insulin sensitivity in both diet-induced and age-induced metabolic dysfunction models 1. NMRK1 expression is downregulated in response to high-fat diet and aging 1. Beyond hepatic metabolism, NMRK1 is a BMAL1-regulated circadian gene in mouse liver, exhibiting rhythmic expression patterns that are lost in BMAL1-knockout models, linking circadian clock function to NAD+ biosynthesis 2. NMRK1 is identified as a shared gene between sarcopenia and type 2 diabetes mellitus pathophysiology 3. Clinically, NMRK1-dependent NAD+ synthesis represents a compensatory pathway in cancer cells resistant to NAMPT inhibitors, with NMRK1 silencing failing to restore sensitivity to such inhibitors in triple-negative breast cancer models 4. These findings establish NMRK1 as a therapeutically relevant target for metabolic diseases and highlight its role in NAD+-dependent cellular adaptation.