Moreover, members of the ACSS subfamily—such as ACSS2—are highly upregulated in cisplatin-resistant bladder cancer cells; inhibition of ACSS2 activity reduces de novo fatty acid synthesis by over 60%, and concurrent decreases in palmitoylation levels impair cell migration and proliferation processes regulated by specific palmitoylated proteins [131]. Here, ACSS2 is linked to urinary bladder carcinoma.