DAB1 has recently been reported to act as an effector downstream of Netrin and its receptor deleted in colorectal cancer (DCC) (Zhang et al., 2018), but given that Dab1 null, Apoer2/Vldlr double mutant and reeler mice have very similar phenotypes in mDA neuron development (Nishikawa et al., 2003; Kang et al., 2010; Sharaf et al., 2013), we assume that the phenotype caused by the specific inactivation of Dab1 in mDA neurons will primarily reflect its function downstream of Reelin signaling. Here, VLDLR is linked to colorectal cancer.