In an exploratory analysis using pre-treatment samples from both SCLC and extrapulmonary SCNEC, most responders exhibited high neuroendocrine differentiation, such as ASCL1 or NEUROD1 subtypes, and somatic copy number alterations in genes driving replication stress, including CCNE1 gain and ARID1A loss [194]. This evidence concerns the gene CCNE1 and small cell lung carcinoma.