NM_000368.5:c.1438+6G>A is present in gnomAD at very low allele frequency (0.010% in v2.1, 0.015% in v4.1; 28–243 alleles, no homozygotes), meeting PM2 at supporting strength.¹ The variant is reported in ClinVar (ID 48782) with 10 of 15 clinical laboratory submissions classifying as Benign or Likely Benign, meeting BP6 at supporting benign strength. No submission classifies as Pathogenic.² SpliceAI predicts no significant splicing impact (max delta score 0.10). No other computational or functional evidence supports or refutes a deleterious effect.³ PS2 (de novo), PS3 (functional), PS4 (case-control), PM6 (assumed de novo), PP1 (cosegregation), PP4 (patient phenotype), BS2 (healthy adults), BS3 (benign functional), BS4 (lack of segregation), BP2 (in trans/cis), and BP5 (alternate molecular basis) could not be assessed due to absence of variant-specific clinical or functional data. PVS1 is not met: the variant is at the +6 intronic position outside canonical ±1,2 splice sites, and SpliceAI does not predict a splice alteration. The variant does not qualify as a predicted null variant under ClinGen SVI PVS1 recommendations.⁴ Using the generic ACMG/AMP 2015 combination rules (PMID:25741868), the variant has one supporting pathogenic criterion (PM2) and one supporting benign criterion (BP6). The net point score is 0, resulting in a classification of Variant of Uncertain Significance (VUS). This is consistent with the conflicting ClinVar aggregate classification.⁵