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Beyond Gemini-3-Pro: Revisiting LLM Routing and Aggregation at Scale

arXiv:2601.01330v1 Announce Type: new Abstract: Large Language Models (LLMs) have rapidly advanced, with Gemini-3-Pro setting a new performance milestone. In this work, we explore collective intelligence as an alternative to monolithic scaling, and demonstrate that open-source LLMs' collaboration can surpass Gemini-3-Pro. We first revisit LLM routing and aggregation at scale and identify three key bottlenecks: (1) current train-free routers are limited by a query-based paradigm focusing solely on textual similarity; (2) recent aggregation methods remain largely static, failing to select appropriate aggregators for different tasks;(3) the complementarity of routing and aggregation remains underutilized. To address these problems, we introduce JiSi, a novel framework designed to release the full potential of LLMs' collaboration through three innovations: (1) Query-Response Mixed Routing capturing both semantic information and problem difficulty; (2) Support-Set-based Aggregator Selection jointly evaluating the aggregation and domain capacity of aggregators; (3) Adaptive Routing-Aggregation Switch dynamically leveraging the advantages of routing and aggregation. Comprehensive experiments on nine benchmarks demonstrate that JiSi can surpass Gemini-3-Pro with only 47% costs by orchestrating ten open-source LLMs, while outperforming mainstream baselines. It suggests that collective intelligence represents a novel path towards Artificial General Intelligence (AGI).

Single-Cell Multi-Omics in Type 2 Diabetes Mellitus: Revealing Cellular Heterogeneity and Mechanistic Insights

Int J Mol Sci. 2025 Nov 13;26(22):11005. doi: 10.3390/ijms262211005.

ABSTRACT

Type 2 diabetes mellitus (T2DM) is a prevalent and complex metabolic disorder characterized by insulin resistance, progressive β-cell dysfunction, and severe systemic complications. Advances in single-cell multi-omics-transcriptomics, chromatin accessibility profiling, and integrative analyses-have offered unprecedented insights into the cellular heterogeneity and regulatory networks of pancreatic islets. We highlight recent discoveries in islet cell heterogeneity and β-cell pathophysiology, with a particular focus on dysfunction and dedifferentiation. We further underscore the computational frameworks that enable these discoveries, spanning data preprocessing, multi-omics integration, and machine learning-driven analyses, which collectively enable the dissection of disease-relevant cell subpopulations and the reconstruction of developmental and regulatory trajectories. We also examine how impaired signaling within islets and chronic adipose inflammation contribute to T2DM pathogenesis. Finally, we discuss key challenges in clinical translation-including limited population diversity in single-cell atlases and the interpretability of computational models-and propose future directions toward precision diagnostics and therapeutic innovation in T2DM.

PMID:41303487 | PMC:PMC12652634 | DOI:10.3390/ijms262211005

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