LDLR and breast carcinoma: As more direct evidence, this investigation showed that the reduction or inhibition of TA-MUC1 activity resulted in significant alterations to a number of the signalling pathways and proteins relevant to abnormal cholesterol metabolism—this signature includes proteins for cholesterol and fatty acid synthesis/deposition (e.g., leptin, LDLR, Apo B) and lipid transport (e.g., ABCA1, ACAT1), as well as the crucial regulators of foam cell formation (e.g., KLF4), a consequence of which was that cholesterol metabolism was reduced by reducing or inhibiting the TA-MUC1 gene in breast cancer cells.