MLCK and ROCK can independently regulate cell polarization. The Rho–ROCK–myosin pathway has previously been found to play a role in regulating large-scale cell polarity by acting at the cell rear, such that decreasing myosin activity increases the protrusion number. We propose that a MLCK–myosin pathway can also regulate cell polarity by acting at the cell front to directly control protrusion lifetime and size. Our results show that decreasing MLCK activity decreases protrusion number.