Considering in particular the antigen presentation phase, preclinical data showed that SCLC has a low intrinsic expression of MHC class I and II molecules [140, 141], and one of the underlying mechanisms behind this consists of epigenetic modifications, as demonstrated by the restoration of MHC class I expression as well as the T cell-mediated killing of tumour cells due to the pharmacological inhibition of EZH2 in SCLC cell lines [142]. The gene discussed is EZH2; the disease is neoplasm.