A specific SF3B1 sequence change was not resolved, so this case could not be linked to variant-specific somatic observations or germline disease database entries. Population evidence could not be assessed because no genomic coordinates or allele frequency data were available for comparison with ACMG/AMP frequency thresholds. No variant-specific functional studies were identified, and generic PVS1 could not be applied because both the exact variant consequence and gene-level loss-of-function eligibility remained unresolved.¹ In silico evidence could not be assessed because no resolvable variant was available for SpliceAI, REVEL, BayesDel, or same-residue PM5 comparison.²