The　PML::RAR　alpha　fusion　gene　resulting　from　the　t(15;17)　chromosomal　translocation　serves　as　the　pathognomonic　molecular　marker　of　acute　promyelocytic　leukemia　(APL),　which　has　been　shown　to　directly　repress　transcription　of　retinoic　acid　(RA)-responsive　genes,　ultimately　inducing　granulocytic　differentiation　arrest.　In　this　study,　we　report　an　APL　case　harboring　an　atypical　PML::RAR　alpha　fusion　transcript　characterized　by　a　novel　splice　site　variant　(GCCaggccc)　within　PML　exon　6,　resulting　in　an　80　base　pairs　deletion　of　the　distal　exonic　sequence　with　concomitant　insertion　of　23　exogenous　nucleotides　(agagccttcttctctctgggacaag).　To　our　knowledge,　this　isoform　differs　from　all　previously　described　PML::RAR　alpha　fusion　transcripts.　This　case　emphasizes　the　importance　of　molecular　characterization　in　APL　diagnosis　and　minimal　residual　disease　(MRD)　monitoring,　though　further　studies　are　required　to　establish　its　clinical　correlation.