Two in vivo studies showed conflicting results: one claimed KMT2C has a carcinogenic role and reported an overexpression in prostate cancer than in normal tissues (did not show survival data) [23]; another one claimed the truncated KMT2C a driver of tumor development and used public data to display a negative prognostic indication of KMT2C-loss [24]. This evidence concerns the gene KMT2C and prostate cancer.