FOSL1 and neoplasm: Taking advantage of p18;Gata3 double mutant mouse models, in which depletion of Gata3 converts p18 deficient luminal tumors into BLBCs with EMT features and enrichment of CSC characteristics [15, 16], we demonstrated that deficiency of Gata3 activates Fosl1 transcription and concurrently represses Fos transcription in the activation of EMT, driving tumor initiation and metastasis.