To determine the role of the GT3-INCP–GATA3 interaction in mediating the tumor-promoting function of GT3-INCP, we performed rescue experiments to investigate whether the inhibition of ER+ luminal BC cell growth and colony formation caused by siRNA-mediated LINC00992 depletion can be reversed by overexpressing wild-type GT3-INCP or the Del-M8 mutant that showed a defective interaction with GATA3. Here, GATA3 is linked to neoplasm.