Adcy7, short for adenylate cyclase 7, is an enzyme that converts ATP to cAMP. It is involved in G protein-coupled receptor signaling pathways. Its function is crucial in various biological processes as it can influence cell growth, apoptosis, and immune responses [2]. Gene knockout models, like the ones used in research, can help reveal its role in specific biological functions and disease conditions.

In hepatocellular carcinoma (HCC), a genome-wide in vivo CRISPR screen identified ADCY7 as a novel immune modulator. The transmembrane protein ADCY7 translocates to the nucleus, where it acts as a transcription cofactor of CEBPA to induce CCL5 transcription, increasing CD8+ T cell infiltration and restraining HCC progression. Exosomes with high ADCY7 levels also suppress HCC tumor growth [1].

In acute myeloid leukemia (AML), inhibition of ADCY7 using an shRNA-encoding lentivirus system in human AML cells led to decreased cell growth, elevated apoptosis, and lower c-Myc expression, suggesting that ADCY7 supports AML development [2].

In a patient with congenital hyperinsulinism (CHI), compound heterozygous variants in ADCY7 were identified. Nuclease technology-mediated ADCY7 knockout in the RIN-m cell line led to increased insulin secretion and activation of the glucose-stimulated insulin secretion pathway [3].

In conclusion, Adcy7 plays essential roles in immune-related processes in HCC, development of AML, and insulin secretion in CHI. Gene knockout models have been instrumental in revealing these functions, providing potential therapeutic targets for these diseases.