Our results revealed that BMAL1-KD, in addition to E-cadherin and EpCAM, increased membranous expression of several cell surface proteins implicated in the matrix–cell adhesion [31,32] and the apico-basolateral polarity [36] of CRC cells such as integrin β1 (CD29), integrin α5 (CD49e), and CD44. The gene discussed is ITGA5; the disease is colorectal carcinoma.