FSTL1 knockdown facilitated ccRCC cell growth, migration, invasion, and promoted cell cycle, possibly because a low level of FSTL1 was unable to repress some cancer-promoting force(s); overexpression of FSTL1 did not inhibit the growth and invasion, possibly because FSTL1 expression at the normal level was enough to repress the cancer-promoting force(s), thus it should be important to restore the FSTL1 expression level to the normal range for attenuating the growth advantage of ccRCC. The gene discussed is FSTL1; the disease is cancer.