Engreitz Lab · Stanford Medicine

Every heartbeat is written in the code of the genome.

We're mapping the regulatory wiring of the heart — cell by cell, switch by switch — to understand congenital and adult heart disease and to build a new generation of genetic cures.

Our genome contains two million regulatory switches that decide when each of our 21,000 genes turns on. Get the wiring wrong, and disease follows. We are building the map of that wiring in the human heart — and using it to design a new generation of cures.

  • CRISPR genomics Massively parallel perturbation of the noncoding genome.
  • AI & computation Models that learn the rules of gene regulation from data.
  • Human genetics Turning disease variants into mechanisms and targets.
  • Team science Computational and experimental scientists, side by side.

Two ways in

Whether you build science or believe in it — there's a place for you here.

For scientists

Do science that changes medicine.

We build enhancer maps, learn the language of the genome, and use CRISPR to find disease genes. Come do it with us — or use our data and tools in your own lab.

For supporters

Help us find lasting cures.

Surgeons can patch a heart; we are working to fix the DNA defects underneath. Your support accelerates the search for the first CRISPR therapies for heart disease.

The science, in four scrolls

From three billion letters to a cure.

gene
01

Three billion letters. Barely any of them are genes.

Only ~2% of the human genome codes for proteins. The rest was long dismissed as "junk" — but it holds the instructions for when and where each gene is used.

02

Hidden in between: two million switches.

These are enhancers — short stretches of DNA that turn nearby genes on. Each cell type uses its own combination to build its identity.

03

This is where disease hides.

Over 100,000 genetic variants linked to human disease fall inside these switches — including hundreds for heart disease. But which gene does each one break?

04

We map every switch to its gene — in every cell type.

Using massively parallel CRISPR screens and the Activity-by-Contact model, we trace each enhancer to the gene it controls. The wiring rewires from one heart cell type to the next — switch cell types below to see it move.

By the numbers

The scale it takes to decode the heart.

~2M
regulatory switches

noncoding "words" in the human genome that decide when genes turn on

100
fetal hearts mapped

a genetic atlas of the developing human heart, finished ahead of schedule

~1M
single cells profiled

enough scale to find and read even the rarest cell types in the heart

~100
genome "words" linked to heart-attack risk

found with Perturb-seq — each a possible target for a new drug

8
institutions in the IGVF consortium

UCSF · Harvard · MIT · Broad · Stanford · UCSD · WashU · MSK

The next five years

An agenda to rewrite what's possible in cardiac medicine.

  1. 01

    Enhancer maps in every cell type

    Comprehensive maps of enhancer–gene connections across every cell type in the heart — and, ultimately, the human body.

  2. 02

    Gene-program maps of the heart

    Gene-program maps across the 20 major cell types of the human heart, defining the regulatory logic of each.

  3. 03

    Causal pathways for heart disease

    Causal pathways for 10 major heart diseases, uncovered through genome-wide Perturb-seq.

  4. 04

    A new class of CRISPR therapy

    Prototype CRISPR therapies that reprogram the regulatory genome to treat disease at its source.

The people

Computational and experimental scientists, side by side.

The heart's regulatory code doesn't respect disciplinary lines, so neither do we. Our team is trained at the intersection of genomics and heart disease — biologists who code, engineers who run CRISPR screens, and computational scientists fluent in the wet lab. Training the next generation of scientists is central to everything we do.

Meet the team
  • Genomics
  • Computer science
  • Bioengineering
  • Biology
  • Human genetics

Supported by

Broad InstituteNIH