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| Main Authors: | , , , , |
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| Format: | Preprint |
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2025
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| Online Access: | https://arxiv.org/abs/2510.10238 |
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| _version_ | 1866911433197879296 |
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| author | Qin, Zixuan Yu, Qingchen Lyu, Kunlin Fan, Zhaoxin Sun, Yifan |
| author_facet | Qin, Zixuan Yu, Qingchen Lyu, Kunlin Fan, Zhaoxin Sun, Yifan |
| contents | Large Language Models (LLMs) have become foundational tools in natural language processing, powering a wide range of applications and research. Many studies have shown that LLMs share significant similarities with the human brain. Recent neuroscience research has found that a small subset of biological neurons in the human brain are crucial for core cognitive functions, which raises a fundamental question: do LLMs also contain a small subset of critical neurons? In this paper, we investigate this question by proposing a Perturbation-based Causal Identification of Critical Neurons method to systematically locate such critical neurons in LLMs. Our findings reveal three key insights: (1) LLMs contain ultra-sparse critical neuron sets. Disrupting these critical neurons can cause a 72B-parameter model with over 1.1 billion neurons to completely collapse, with perplexity increasing by up to 20 orders of magnitude; (2) These critical neurons are not uniformly distributed, but tend to concentrate in the outer layers, particularly within the MLP down\_proj components; (3) Performance degradation exhibits sharp phase transitions, rather than a gradual decline, when these critical neurons are disrupted. Through comprehensive experiments across diverse model architectures and scales, we provide deeper analysis of these phenomena and their implications for LLM robustness and interpretability. These findings can offer guidance for developing more robust model architectures and improving deployment security in safety-critical applications. Our code is available at https://github.com/qqqqqqqzx/The-Achilles-Heel-of-LLMs. |
| format | Preprint |
| id |
arxiv_https___arxiv_org_abs_2510_10238 |
| institution | arXiv |
| publishDate | 2025 |
| record_format | arxiv |
| spellingShingle | The Achilles' Heel of LLMs: How Altering a Handful of Neurons Can Cripple Language Abilities Qin, Zixuan Yu, Qingchen Lyu, Kunlin Fan, Zhaoxin Sun, Yifan Artificial Intelligence Large Language Models (LLMs) have become foundational tools in natural language processing, powering a wide range of applications and research. Many studies have shown that LLMs share significant similarities with the human brain. Recent neuroscience research has found that a small subset of biological neurons in the human brain are crucial for core cognitive functions, which raises a fundamental question: do LLMs also contain a small subset of critical neurons? In this paper, we investigate this question by proposing a Perturbation-based Causal Identification of Critical Neurons method to systematically locate such critical neurons in LLMs. Our findings reveal three key insights: (1) LLMs contain ultra-sparse critical neuron sets. Disrupting these critical neurons can cause a 72B-parameter model with over 1.1 billion neurons to completely collapse, with perplexity increasing by up to 20 orders of magnitude; (2) These critical neurons are not uniformly distributed, but tend to concentrate in the outer layers, particularly within the MLP down\_proj components; (3) Performance degradation exhibits sharp phase transitions, rather than a gradual decline, when these critical neurons are disrupted. Through comprehensive experiments across diverse model architectures and scales, we provide deeper analysis of these phenomena and their implications for LLM robustness and interpretability. These findings can offer guidance for developing more robust model architectures and improving deployment security in safety-critical applications. Our code is available at https://github.com/qqqqqqqzx/The-Achilles-Heel-of-LLMs. |
| title | The Achilles' Heel of LLMs: How Altering a Handful of Neurons Can Cripple Language Abilities |
| topic | Artificial Intelligence |
| url | https://arxiv.org/abs/2510.10238 |