Here’s what you’ll learn when reading this story:

• For decades, the “classical view” of genetics has hewn closely to the original work of Austro-Hungarian biologist Gregor Mendel, who developed his laws of inheritance in the mid-1880s.
• A new study suggests that while Mendelism gave us wondrous insight into the world of genetics, it alone cannot explain genetic variation across a population, or how certain genomes produce certain phenotypes.
• The new research embraces the idea of genome-wide association studies and calls for the further acceptance of polygenicity—the idea that multiple genes can impact a phenotypic trait or disease.

Between 1856 and 1863, Austro-Hungarian friar and biologist Gregor Mendel cultivated and tested 28,000 pea plants—most of which belonged to the species Pisum sativum—in the garden of the Augustinian Abbey of St. Thomas in Brno. From these experiments, Mendel worked out the ideas of dominant and recessive genes, as well as his laws of inheritance. This concept is most commonly referenced in high school biology class using the Punnett square (named for British geneticist Reginald Punnett, who developed the system and authored one of the first books on genetics, Mendelism).

Mendel’s work helped establish important genetic concepts even before people knew that genes existed. But now, a new study posits that the prevailing view of Mendelian inheritance was eventually overshadowed by the work of English polymath Francis Galton, who instead focused on the inheritance of continuous variation. A recent study in the journal Genetics refers to Galton’s original view as the “biometric school” of heredity. The term biometric refers to the statistical measurement of biological traits, and Galton's school held that traits like height varied continuously across populations, rather than being inherited as the discrete units Mendel described. In the context of this new research, that biometric perspective has matured into the field of quantitative genetics, which uses large-scale genomic data to show that most traits arise not from one or a few genes but from complex networks of thousands of interdependent genes, each contributing a small effect.

However, Mendelism—with its more elegant explanations and simple Punnett squares—largely won the conversation, and became the dominant view on genetics for more than a century. The researchers behind the new study, who come from institutions across Europe and the U.S., are wondering if it’s time to move beyond Mendel and embrace the true complexity of genetic variation.

“The long-standing notion that genotypes map to phenotypes through simple one gene–one trait relationships continues to shape both research in the life sciences and public understanding, with implications for policy and funding priorities,” the authors write. “Yet this paradigm is increasingly recognized as inadequate for explaining continuous phenotypic variation and the complex genetic architectures of the genotype–phenotype map.”

The authors don’t advocate for abandoning Mendelism entirely—after all, it’s led to stunning technological breakthroughs like gene editing and provided a framework for gene pathways. But the Mendelian approach doesn’t provide enough explanatory power to discern phenotypic variation across entire populations, nor does it allow scientists to ascertain why certain genomes express certain physical characteristics. In 2025, for example, scientists successfully characterized all seven loci that Mendel identified in his original pea plant experiments some 160 years ago. But they also included 72 additional traits governed by a few genes (oligogenic traits) or even many genes (polygenic traits).

“This contrast shows most directly that the single-gene genetics that is based on Mendelian approaches reveals only a partial insight into the generation of the phenotype,” the authors wrote.

This isn’t the first call for researchers to embrace a broader view of the genetic landscape. Efforts in the 1930s and 1940s to unite Mendelian inheritance with Darwinism—known as the “Modern Synthesis”—underlined this genetic complexity. And more recently, studies known as genome-wide association studies (GWAS) have similarly attempted to look at genetic variation through a more complicated, global lens.

“Yet, these attempts have failed to convince many molecular biologists who remain resistant to the idea that polygenicity can provide meaningful mechanistic insights,” the authors wrote. “We call once again for the community of researchers that engages in more classical genetics to also embrace the complexities of genotype–phenotype mapping and ask them to appreciate the need for the development of experimental genetic approaches that assess mechanism through the lens of polygenicity.”