RBIS (ribosomal biogenesis factor) is a trans-acting factor required for efficient production of both 40S and 60S ribosomal subunits, functioning primarily in the nucleolus and nucleoplasm 1. Mechanistically, RBIS regulates ribosome biogenesis by controlling 47S ribosomal RNA (rRNA) expression, a critical component of ribosome assembly, and interacts with the ribosomal maturation factor GNL2 as a key downstream regulator 1. RBIS expression directly affects protein translation efficiency and global protein synthesis rates, as demonstrated through polysome profiling and fluorescence-based assays 1. Clinically, RBIS is significantly upregulated in lung adenocarcinoma, where high expression correlates with poor prognosis and enhanced tumor progression 1. Functionally, RBIS knockdown inhibits cancer cell migration, invasion, and proliferation while inducing G0/G1 cell cycle arrest and apoptosis in lung cancer cells 1. Additionally, RBIS downregulation synergizes with ribosomal biogenesis-targeting drugs like CX-5461 to suppress cell cycle progression and increase apoptosis, and importantly, RBIS knockdown substantially enhances chemosensitivity to gemcitabine 1. These findings suggest RBIS represents a promising therapeutic target for lung adenocarcinoma treatment.