Notably, exploration of the mechanism by which circPCLE1 modulated CRC glycolysis manifested that it functioned through the competitive adsorption of miR-485-5p to mediate ACTG1, which further emphasized that ACTG1 is vital in cancer glycolysis and supposed to be a new target for repressing cancer glycolysis later. The gene discussed is ACTG1; the disease is colorectal carcinoma.