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Hematologic

Sideroblastic Anemia 2

Assembled from catalogue records November 5, 2026

Sideroblastic Anemia 2, as genome-wide studies have reported it: 28 positions from 1 study. Built from the GWAS Catalog's records and rebuilt when a new position is reported; the figures are the studies'.

What this condition connects to

Prevalence
Not taken from these records, which report study sizes rather than how common the condition is.
Inheritance
The records show a polygenic pattern — 28 positions from 1 study, each a common variant of small effect. How much of Sideroblastic Anemia 2 is inherited is not something they measure.

Sideroblastic Anemia 2 — filed in the GWAS Catalog as "Sideroblastic anemia 2" — is a condition this catalogue follows as its positions arrive. This page is assembled by MyGeneLog's own code from the catalogue's records and the studies' own listings: 28 positions from 1 study, and no sentence written by hand. It is rebuilt as new positions are reported, so what it says is what the records say today.

The studies behind the positions

A study. It contributes 28 positions: rs1156987118 (SLC25A38), rs1198314410 (SLC25A38), rs1218815001 (SLC25A38), rs121918330 (SLC25A38), rs121918332 (SLC25A38), rs1233124208 (SLC25A38), rs1293528130 (SLC25A38), rs1448237170 (SLC25A38), and 20 more.

Positions and mapped genes

The 28 positions lie in or near 1 gene: SLC25A38. A gene named here is the catalogue's mapped location for a position, not a mechanism; the studies are cited above so that a reader can go to them.

Reading this page

Association records say which positions differ, on average, between people with Sideroblastic Anemia 2 and people without. They do not describe the condition, say how common it is, or tell anyone what to do, so this page does not either. For a single position, open its variant page: it gives that study's record in fixed sentences, with ClinVar's where there is one.

Clinical detail

Genotype and diagnosis

Nothing on this page diagnoses Sideroblastic Anemia 2. The 28 variants here are research findings; no guideline uses them to predict, screen for or diagnose the condition — that is a clinician's work.

Everything here comes from population-level association records, put together by code. Those records compare groups of people; they do not examine anyone, and they give no guidance on care. For symptoms, testing or treatment, ask a clinician.

Sources

Databases, guidelines and references

Quoting this page

Licensed CC BY-NC 4.0: free to read, share and adapt for non-commercial use, naming MyGeneLog™ and linking the exact page. Commercial use, including training or serving a commercial AI system, needs a licence — https://www.mygenelog.com/license

Sideroblastic Anemia 2. MyGeneLog™. https://www.mygenelog.com/conditions/sideroblastic-anemia-2

Questions about Sideroblastic Anemia 2

What is Sideroblastic Anemia 2?

Sideroblastic Anemia 2 is the condition the GWAS Catalog files under "Sideroblastic anemia 2". This page does not define it in its own words; it lists what genome-wide studies have reported: 28 positions from 1 study, with each study's sample and citation.

Is Sideroblastic Anemia 2 genetic?

Genome-wide studies have reported 28 associated positions. Each common variant has a small effect, and an association in a population is not a cause in any one person.

Which genes are linked to Sideroblastic Anemia 2 on this page?

The positions lie in or near 1 gene: SLC25A38. A mapped gene is the catalogue's location for a position, not a mechanism.

Can these variants predict whether I will get Sideroblastic Anemia 2?

No. Each variant shifts the odds only slightly, and only on average across many people. No guideline predicts Sideroblastic Anemia 2 from a genotype; a clinician diagnoses it.

Free to reuse, non-commercially. This page's text is original writing from freely-available research, licensed CC BY-NC 4.0 — share and adapt it with attribution to MyGeneLog™; commercial use is licensed. It's general research-derived information, not medical advice or a diagnosis — see Terms of Use.