Such data could be clarified in two theories: wrong selection of gene promoter sequence to analyse; or different gene regulation mechanisms than promoter methylation is intrinsic for CHI3L1. Recent discoveries found that CHI3L1 acts on glioblastoma-stem like cells (GSCs) to drive the formation of tumour vascularization and targeting CHI3L1 may compliment conventional anti-angiogenic therapies to provide a substantial clinical benefit to patients with GBM [15]. The gene discussed is CHI3L1; the disease is glioblastoma.