PROM1 and neoplasm: Recently, it has been reported that treatment of lactate in hepatocellular carcinoma cells promotes CD133 expression, induces Nanog, Oct4 and SOX2 genes expression and increases sorafenib resistance [32], and targeting LDHA by siRNAs markedly decreases spheroid formation capacity and reduces the expression of CSC genes and mesenchymal markers in cancers [32, 33], suggesting that LDHA facilitates aerobic glycolysis and might produce lactate to alter CSC characteristics and promote tumour progression.