The PTEN c.898dup (p.Ile300AsnfsTer3; p.I300Nfs*3) variant has not been observed in COSMIC and has not been reported in ClinVar; OncoKB classifies it as likely oncogenic with a likely loss-of-function effect.¹ This variant is absent from gnomAD v2.1 and gnomAD v4.1, which is below the PTEN PM2_Supporting threshold of 0.001% and is consistent with rarity in the general population.² This frameshift introduces a premature stop codon upstream of the PTEN-specific p.D375 (c.1121) threshold in NM_000314.8, which is consistent with predicted nonsense-mediated decay and supports PVS1 at very strong strength under the PTEN-specific decision tree.³ SpliceAI predicts no significant splice impact for this variant, with a maximum delta score of 0.01, indicating that the primary predicted effect is protein truncation rather than altered splicing.⁴