This two-base-pair deletion in TP53 exon 6 produces a frameshift (p.Asn200IlefsTer8) with a premature termination codon at approximately codon 207, upstream of p.Lys351 and predicted to undergo nonsense-mediated decay, satisfying PVS1 at very strong strength per the TP53 VCEP decision tree.¹ The variant is absent from gnomAD v2.1, v4.1, and gnomAD-Canada, meeting PM2_Supporting at an allele frequency below 0.003%.² Absence from population databases is consistent with a pathogenic role and does not satisfy any benign frequency criterion (BA1, BS1).³ No variant-specific functional, segregation, de novo, or clinical observations were identified, and none of the reviewed publications mentions NM_000546.6:c.599_600del; therefore no additional pathogenic or benign criteria are met.⁴