Furthermore, Top2 inhibitors like etoposide are able to stimulate genomic aberration in cancer cells and both Top1 and Top2 inhibitors are able to induce transcription of STING-dependent chemokines like CCL5 and CXCL10 (Fig. 1), disclosing a possible role of these compounds as drugs that can trigger an innate immune response, a key point for immunotherapy efficacy in unresponsive tumours such as SCLC subtypes [89–91]. The gene discussed is TOP2A; the disease is small cell lung carcinoma.