The mechanism mainly shows that inhibition of Cav-1 can reduce the binding of the E3 ligase VHL to C-myc, alleviate the ubiquitination degradation of C-myc protein, and promote the accumulation of C-myc, thus leading to the orderly progress of aerobic glycolysis mediated by C-myc and providing energy support for the self-renewal ability of breast cancer stem cells. The gene discussed is CAV1; the disease is breast carcinoma.