PCSK7 is a serine endoprotease that processes proproteins by cleaving at paired basic amino acid motifs, functioning primarily in the constitutive secretory pathway and trans-Golgi network. Beyond its canonical enzymatic role, PCSK7 exhibits noncanonical functions as a post-translational regulator of apolipoprotein B, making it distinct among the nine-member proprotein convertase family 1. PCSK7 has emerged as a key regulator of metabolic and cardiovascular disease. Genetic variants in PCSK7 associate with dyslipidemia and acute coronary syndrome risk, with the rs236918 C allele linked to higher triglycerides and lower HDL-cholesterol 2. In liver disease, PCSK7 expression correlates with lipogenic gene activity, and elevated hepatic PCSK7 protein promotes triglyceride accumulation and fibrogenesis 3. During myocardial infarction, PCSK7 in macrophages amplifies TNF-α/JNK signaling, intensifying post-infarction inflammation 4. Emerging evidence suggests PCSK7 also regulates immune checkpoint protein expression on CD8+ T cells; PCSK7 deficiency reduces surface levels of LAG3, CTLA4, and PD1 by ≥40%, potentially enhancing anti-tumor immunity 5. Clinically, PCSK7 represents a promising therapeutic target for metabolic dysfunction-associated steatotic liver disease, dyslipidemia, and cardiovascular disease. Mouse knockout studies demonstrate that Pcsk7 deletion produces healthy, fertile animals without apparent toxicity, and synergistic inhibition of PCSK7 and PCSK9 may offer novel treatment strategies 1. PCSK7 inhibition via hepatocyte-targeted antisense oligonucleotides shows efficacy in preclinical models, positioning oligonucleotide-based PCSK7 inhibitors as candidates for clinical development 1.