Combined with the earlier observation of the robust dephosphorylation of MYPT1 late in infection (42 hpi), this result suggests that CT228-mediated MYPT1 recruitment may result in MYPT1 activation instead [127], perhaps serving as a mechanism to regulate myosin II activity at the inclusion (and thereby regulating extrusion-mediated egress of the pathogen). The gene discussed is PPP1R12A; the disease is infection.