CrAT, specifically for short-chain acyl-CoAs conversion, was also reported to be overexpressed in androgen-dependent and androgen-independent prostate tumor cells, and in prostate cancer patient’s biopsies, by Valentino et al. In line with this, a network comprising two members of the carnitine palmitoyltransferase system—CrAT, and CACT, together with CPT1A—makes prostate cancer cells more likely to utilize and oxidate FAs, contributing to the maintenance of their high metabolic plasticity [4,36]. The gene discussed is CPT1A; the disease is prostate carcinoma.