In the first instance, we confirmed the results of the SHM analysis that pathways, described in previous studies as deregulated in glioblastoma pathogenesis, are epigenetically regulated, including pathways related to neoplastic transformation (Receptor Tyrosin Kinase (RTK) signalling (EBRR2) [32], WNT signalling [33], GPCR signalling [34]), neuronal systems (potassium channels [35]), cellular response to stress and ALK signalling [36, 37], as well as genes involved in circadian clock regulation [36, 38, 39] (Additional File 1: Fig.S5e and Additional File 3: table S2). The gene discussed is ALK; the disease is glioblastoma.