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]. The gene discussed is ASCL1; the disease is small cell lung carcinoma.