More specifically, in CRC, circ-ACC1 has been suggested to form a ternary complex with the regulatory β and γ subunits of PRKAA1 (AMPK), stabilizing it and increasing its activation, thereby promoting fatty acid β-oxidation, glycolysis, and growth of CRC cells (Figure 3B) [34]. The gene discussed is PRKAA1; the disease is colorectal carcinoma.