RPS10 is a structural component of the 40S ribosomal subunit essential for protein synthesis 1. As part of the cytosolic small ribosomal subunit, RPS10 participates in ribosomal quality control mechanisms. The G3BP1-family-USP10 complex deubiquitinates RPS10 following ZNF598-mediated monoubiquitination to rescue stalled 40S subunits from lysosomal degradation during ribosome-associated quality control 2. Nitric oxide-induced ribosome collision triggers ZNF598-mediated ubiquitination of RPS10, activating ribosomal surveillance pathways 3. RPS10 also mediates translation initiation through interaction with eIF1A; inhibiting eIF1A-RPS10 interaction selectively impairs cancer cell proliferation and SARS-CoV-2 infection 4. Clinically, RPS10 mutations cause Diamond-Blackfan anemia (DBA), a rare inherited bone marrow failure syndrome 5. RPS10 mutations account for approximately 4% of DBA cases and are associated with lower rates of physical malformations (22%) compared to overall DBA (~50%) 6. Patients with RPS10 mutations show elevated 18S-E pre-rRNA, indicating defective rRNA processing 5. Additionally, Mendelian randomization analysis identified RPS10 as a causal risk factor for postmenopausal osteoporosis 7.