RPL36A encodes a structural component of the large ribosomal subunit involved in protein synthesis 1. Beyond its canonical ribosomal function, RPL36A has emerged as a multifunctional protein with significant disease relevance. In epithelial-mesenchymal transition (EMT), RPL36A is enriched in mesenchymal ribosomes, and its overexpression alone is sufficient to trigger mesenchymal features and alter cell morphology and behavior, demonstrating a pivotal role in EMT progression 1. In cancer contexts, RPL36A expression is consistently upregulated: it is elevated in acute myeloid leukemia (AML) cells where RPL36A knockdown inhibits proliferation and promotes apoptosis 2, overexpressed in hepatocellular carcinoma (HCC) where it correlates with enhanced colony formation and cellular proliferation 3, and identified as a cuproptosis-related risk gene in non-small cell lung cancer (NSCLC) with prognostic value 4. Additionally, RPL36A expression is upregulated by polyamines in cancer cells, particularly in conjunction with eIF5A2, linking it to cancer malignancy 5. In chrX myeloid leukemia, RPL36A is among upregulated ribosomal proteins identified as potential therapeutic targets 6. Notably, a genomic enhancer (GH0XJ101390) regulating RPL36A expression may influence Fabry disease pathology through coordination with the GLA gene in the RPL36-HNRNPH2 region 7. These findings establish RPL36A as both a marker of malignant transformation and a potential therapeutic target across multiple cancer types.