TP53 and neoplasm: Comprehensive genomic profiling revealed a complex molecular landscape: a "double hit" driving hypercortisolism (<i>GNAS</i> activation and <i>HSD11B2</i> alteration) and a high tumor mutational burden (11.6 mutations/megabase) driven by converging instability mechanisms (<i>MSH6, TP53, DAXX, DNMT3A</i>, and <i>KMT2A</i> somatic mutations, and <i>TOP2A</i> overexpression), despite stable microsatellite status.