We studied Prkar2a- haploinsufficient (Prkar2a+/−), Prkar2b- haploinsufficient (Prkar2b+/−), Prkar2a−/− KO, as well as double-heterozygote (Prkar1a+/−x Prkar2a+/-) F1 mice for the development of hematologic malignancies. This evidence concerns the gene PRKAR1A and hematologic disorder.