Our current finding further extends this knowledge, revealing that E2F1 binds to the XIAP BIR2 domain as well as the discovery that Sp1 interacts with the XIAP BIR3 domain, and that Sp1 also acts as an E2F1 upstream transcriptional factor to initiate a crosstalk with E2F1 to promote BC cell invasion. Here, XIAP is linked to breast cancer.