Thus, our findings showing that FASN inhibition blocks anchorage-independent growth of CCN1-overexpressing breast cancer cells in the absence of estradiol while restoring their responsiveness to antiestrogens, strongly suggests that CCN1-driven FASN overexpression might be part of the proangiogenic phenotype which, if recapitulated in vivo, may promote tumor progression. The gene discussed is FASN; the disease is breast carcinoma.