In the absence of ACLY, under nutrient deprivation or stress conditions, cells upregulate ACSS2, enabling cancer cells to utilize acetate to sustain tumor growth (Comerford et al., 2014; Mashimo et al., 2014; Schug et al., 2015) by providing acetyl CoA for fatty acid and phospholipid synthesis and histone acetylation (Zhao et al., 2016). Here, ACSS2 is linked to cancer.