Ribosome biogenesis, driven by RNA Polymerase I (Pol I)–mediated transcription of ribosomal RNA (rRNA), is essential for protein synthesis and cell growth. While MYC is a well-studied oncogenic transcription factor, its direct role in rRNA transcription remains less defined. As a case study, Acute Myeloid Leukemia (AML) cells display elevated rRNA synthesis, suggesting MYC may directly promote Pol I activity. We hypothesized that MYC degradation would decrease ribosome production, alter nucleolar structure, and arrest proliferation. With a degron system in AML cells, we rapidly degraded MYC and quantified rRNA abundance through FISH-Flow. MYC loss rapidly reduced 18S and 28S rRNA levels independent of cell cycle phase, decreased nucleolar size and total/percent nucleolar area per nucleus. Furthermore, MYC loss produced more defined, circular nucleoli without altering nucleolar count, and cell proliferation assays revealed growth arrest within three days of sustained MYC depletion. These findings show that MYC is critical for maintaining rRNA synthesis and nucleolar structure in AML cells such that without it, ribosome biogenesis and cell proliferation rapidly decline. Studying MYC-driven rRNA transcription can shed light on the mechanism by which cell proliferation and protein production are upregulated in malignant cancers.