EML3 (EMAP like 3) is a microtubule-associated protein essential for faithful mitotic cell division. Its primary function is regulating mitotic spindle assembly and ensuring proper chromosome 11 1. Mechanistically, EML3 localizes to spindle microtubules throughout mitosis and accumulates in interphase nuclei 2. EML3 recruits the Augmin complex and γ-tubulin ring complex (γ-TuRC) to existing microtubules, thereby promoting microtubule-based nucleation required for spindle formation 1. This recruitment is regulated by CDK1-mediated phosphorylation at Thr-881 1. EML3 knockdown disrupts proper metaphase chromosome 11, causes kinetochore-microtubule misconnection, and delays cell division 1. Beyond mitotic function, EML3 has emerged as a potential disease-relevant target in pulmonary and colorectal contexts. Genome-wide analyses identify EML3 expression as causally associated with lung function traits (FEV1 and FVC) across multiple tissues 3, with DNA methylation at EML3 loci influencing forced expiratory volume 4. EML3 is also upregulated in colorectal cancer patients responsive to FOLFOX chemotherapy, suggesting potential clinical utility in predicting treatment response 5. DNA methylation changes at EML3 occur upon metformin exposure and during fetal development 67.