Mutations in tumor protein P53 and retinoblastoma 1, along with MYC proto-oncogene, BHLH transcription factor like amplifications, which are key drivers well-established in the pathogenesis of SCLC were consistently detected across all 3 sample types.[6] In contrast, RPTOR independent companion of MTOR complex 2 copy number amplification was identified in tumor tissue and CSF but absent in plasma, possibly indicating a lower circulating tumor burden or a dilution effect within the bloodstream. Here, TP53 is linked to neoplasm.