NM_001128849.1:c.1944-1G>T is a canonical splice acceptor variant (c.1944-1G>T, intron 12) in SMARCA4, a gene for which loss of function is an established disease mechanism for rhabdoid tumor predisposition syndrome type 2 (RTPS2).¹ Under the ClinGen SVI PVS1 decision tree (PMC6185798), canonical ±1,2 splice site variants receive PVS1 at very strong strength when LOF is a confirmed disease mechanism. SpliceAI predicts a high-impact splice alteration (delta score 0.99, acceptor loss 0.99), consistent with disruption of the intron 12 splice acceptor.² The variant is absent from all queried population databases including gnomAD v2.1, v4.1, and gnomAD-Canada, meeting the PM2 criterion at moderate strength (<0.1% allele frequency threshold).³ PP3 is not applied because the splice prediction evidence (SpliceAI) is already accounted for in the PVS1 assessment; the ClinGen SVI PVS1 guidance explicitly prohibits stacking PP3 for the same splice-effect evidence.⁴ Under generic ACMG/AMP 2015 final combination rules (PMID:25741868), PVS1 (Very Strong) plus PM2 (Moderate) yields a classification of Likely Pathogenic.⁵