Interestingly, KO of TNFAIP3 not only abolished cell, mammosphere, and tumor growth induced by AP29187-activated iFGFR1, but also reduced cell, mammoshpere, and tumor growth in the absence of AP29187 treatment when compared with the tumors derived from DCIS-iFGFR1 cells with wild-type TNFAIP3. This may be explained by the role of TNFAIP3 in mediating the cell growth function of the endogenous FGFRs and/or the additional functions of TNFAIP3 involved in other cell growth-promoting pathways. The gene discussed is TNFAIP3; the disease is ductal breast carcinoma in situ.