Silencing of SCD inhibits lipid synthesis and activates AMP-activated protein kinase (AMPK; also known as PRKAA2), which in turn increases β-oxidation of fatty acids (Dobrzyn et al., 2004), leading to tumour size reduction in xenograft models of liver (Budhu et al., 2013), lung (Scaglia and Igal, 2008) and stomach (Roongta et al., 2011) cancers, as well as to inhibition of prostate cancer progression in mice (Fritz et al., 2010). This evidence concerns the gene PRKAA2 and neoplasm.