Structure is not mechanism: high-gain gated-FFN rows across text and genomic foundation models

Abstract

A small number of unusually high-gain parameters can exert disproportionate effects in transformer language models, but whether analogous structures recur in genomic foundation models and whether structural geometry determines functional importance remains unknown. We analyzed high-gain rows in gated feed-forward networks across text and genomic foundation models, including a frozen 22-model causal census. Computing an associated bilinear weight operator exactly, without a diagonal approximation, we tested whether structural extremeness is a transferable mechanism. Activation-derived candidates were functionally enriched relative to random and top-norm same-layer controls, yet neither spectral concentration nor operator magnitude predicted causal effect size, and these associations vanished within the endpoint-homogeneous text-decoder subset. A within-layer sweep of 36 rows in one genomic and one text decoder resolved this into two regimes: below the detector's acceptance threshold the ratio carried no positive information about causal damage, whereas above it the ratio ordered rows strongly but did not grade severity as a dose-response. The same sweep revealed a second individually catastrophic row invisible to a one-candidate-per-model census, and non-additive damage among co-located critical rows. Case studies showed divergent causal organizations: a robust super-additive pair interaction in DNABERT-2, and in GENERator a sharply position-localized dependence in which preserving or restoring the row's beginning-of-sequence contribution rescued essentially all native-loss damage. High-gain gated-FFN rows are therefore a recurrent architectural phenotype whose structural prominence acts as an enrichment signal, not a calibrated measure of functional criticality or a specification of causal organization. Enrichment is general, but the mechanism is model-specific.