HME1 cells with genetic mutations hampering the physiological RA regulation of the RA receptor alpha (RARA) transcriptional function, but retain the RARA function controlling the PI3KCA-AKT signaling, develop 3D “DCIS-like” amorphous structures with upregulated ANXA8. The gene discussed is AKT1; the disease is ductal breast carcinoma in situ.