In conjunction with our data showing the hypermethylation of nonpromoter CpGs in MGMT, which have been shown to correlate with MGMT expression in NAFLD, this may imply the loss of expression of MGMT in HCC may be initiated by non‐promoter methylation changes acquired during CLD, which become ‘locked‐in’ by promoter methylation, as has been reported in HCC [11, 80]. The gene discussed is MGMT; the disease is metabolic dysfunction-associated steatotic liver disease.