PRKAR1A and myxoma: The majority of PRKAR1A defects are premature stop codons generated by nonsense, missense or frameshift (insertions, deletions or splice-site modifications) mutations.33 Additionally, the degradation of mutant mRNAs via nonsense-mediated decay was shown to be the cause of PRKAR1A haploinsufficiency,34 which then activates cAMP signaling and promotes downstream cellular processes that lead to tumorigenesis.35 Therefore, the present study demonstrates the occurrence of PRKAR1A mutation in myxoma specimens of four sporadic cardiac myxoma cases without CNC or a family history of cardiac myxoma.