Ustilago maydis is a biotrophic fungus that infects arial parts of maize, secreting effector proteins to facilitate host colonization and manipulate cellular processes, creating nutrient-rich environments for its growth and reproduction. Here, we identified three effectors (Hap1-3; hypertrophy-associated proteins 1-3) as U. maydis virulence factors involved in the development of hypertrophic mesophyll tumor cells (HTT). Immunoprecipitation followed by mass-spectrometry revealed interactions among Hap effectors within host cells, suggesting potential effector complex formation. To study Hap effectors, triple frameshift U. maydis knockout for hap1, hap2, and hap3 was generated using CRISPR-Cas9. Infection assays and mass-spectrometry identified Hap1 as a key HTT-related virulence factor that interacts with maize Snf1-related protein kinase 1 (SnRK1), a central energy homeostasis regulator. RNA-seq analysis showed that Hap1 promotes cell cycle and starch biosynthesis genes, while CR-hap1 induced defense-related WRKY transcription factors. Phosphoproteomics revealed increased phosphorylation of SnRK1 and metabolic enzymes during SG200 infection. Our findings support a model where U. maydis induces hypertrophy through Hap1, targeting the SnRK1α subunit to prevent SnRK1 inhibition by high trehalose-6-phosphate (T6P), disrupting the antagonistic relationship between T6P and SnRK1. This reprograms host transcription to enhance starch metabolism and induce endoreduplication, leading to HTT formation while suppressing sugar-induced immune signaling.