Given that PI3K/AKT signaling pathway was activated by ARID1A knockout or silencing (Figs. 6C, E and S6B), and inactivated by ectopic overexpression of ARID1A in CRC cells (Fig. 6D, F), PI3K could be a potential mediator of the regulatory relationship between ARID1A and p-MAP4. Here, AKT1 is linked to colorectal carcinoma.