PRKAR1A variants are commonly the sole pathogenic genomic finding in clinically benign LCCSCTs without aggressive histopathologic features, whereas clinically malignant tumours tend to harbour additional alterations, including mutations, chromosomal aneuploidies and homozygous deletion of tumour suppressors (e.g., CDKN1B/2A/2B), among others.67, 77. This evidence concerns the gene CDKN1B and neoplasm.