FAM53B, variants, traits, and what the research shows

FAM53B - what this gene does

FAM53B (Family With Sequence Similarity 53 Member B) is a human gene whose catalogued variants point to two broad research areas: pharmacogenomics (the study of how genetic variation shapes an individual's response to drugs) and neurological traits, based on population-level genetic association data.

Key takeaways

• FAM53B carries variants linked to both pharmacogenomics and neurological traits in genetic research databases.
• Four variants reach the highest observed signal magnitude on file, suggesting relatively robust or widely-studied associations.
• 97 variants are catalogued across this gene, with 29 carrying prior research summaries.
• These are population-level statistical signals - they do not predict outcomes for any individual.
• Detailed trait and cohort metadata for several top-ranked variants are not yet fully available in current records.

Notable variants

The four variants with the highest signal magnitude (4.50) are rs10901811, rs11245344, rs11818135, and rs4962693. Of these, rs10901811 is explicitly tagged with a pharmacogenomics trait, and rs4962693 is linked to a neurological phenotype. rs11245344 and rs11818135 carry the same magnitude and have published research pages, though specific trait labels are not available in the current data. A secondary cluster - including rs1044885132, rs1429776106, rs148677670, rs2495552882, and rs367682100 - reaches a magnitude of 3.00.

Trait associations

The available metadata places this gene at the intersection of two research domains. Pharmacogenomics associations are anchored by rs10901811, pointing toward a potential role in drug-response variability. Neurological associations appear through rs4962693. Because the published summaries for rs11245344 and rs11818135 do not include trait-level detail in the current input, the full scope of this gene's associations may be broader than what is described here.

Evidence quality

Of the 97 catalogued variants, 29 carry prior research summaries and four reach a signal magnitude of 4.50 - a level that typically reflects associations reported in large or replicated GWAS (genome-wide association study - a method that scans many thousands of individuals' genomes for statistically significant trait links) analyses. However, detailed cohort sizes, effect sizes, and replication status are not available in the current input for any of the top-ranked variants, limiting the ability to characterize the strength of individual findings. Readers should treat these associations as pointers toward peer-reviewed literature rather than established clinical conclusions.

What this is NOT

All variants described here are population-level statistical signals, not deterministic predictors for any individual. Nothing on this page constitutes medical advice, a diagnosis, or a recommendation of any kind.