NM_005378.6:c.865_867del (p.Ser289del) is an in-frame deletion of a single amino acid in exon 3 of MYCN, a gene in which loss-of-function variants cause autosomal dominant Feingold syndrome type 1.¹ This variant does not meet PVS1 criteria as it is not a null variant (nonsense, frameshift, or canonical splice site).² The variant is present at extremely low frequency in population databases: gnomAD v2.1 AF = 0.00637% (2/31,376 alleles) and gnomAD v4.1 AF = 0.00043% (7/1,613,892 alleles), with no homozygotes observed, meeting PM2 at supporting strength.³ The in-frame deletion changes protein length (p.Ser289del) in a non-repeat region of MYCN, meeting PM4 at moderate strength.⁴ No variant-specific functional studies, segregation data, de novo observations, or case-control evidence are available. ClinVar reports a single classification of uncertain significance.⁵ Computational evidence is limited: SpliceAI predicts no splicing impact (max delta = 0.04), and REVEL/BayesDel are not applicable to deletions. PP3 and BP4 are not met.⁶ Overall classification: Uncertain Significance. One moderate criterion (PM4) and one supporting criterion (PM2) are met, which is insufficient to reach likely pathogenic or likely benign under the ACMG/AMP 2015 framework.⁷