Large sample size and nonlinear sparse models outline epistatic effects in inflammatory bowel disease.

Abstract excerpt

BACKGROUND: Despite clear evidence of nonlinear interactions in the molecular architecture of polygenic diseases, linear models have so far appeared optimal in genotype-to-phenotype modeling. A key bottleneck for such modeling is that genetic data intrinsically suffers from underdetermination ([Formula: see text]). Millions of variants are present in each individual while the collection of large, homogeneous...

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