SUMMARY Meristemoids, which are stomatal precursor cells, exhibit self‐renewal and differentiation abilities. However, the only known core factor associated with meristemoid division termination and fate transition is the heterodimer formed by the basic helix–loop–helix proteins MUTE and SCREAMs (SCRMs). FOUR LIPS (FLP), a well‐known transcription factor that restricts guard mother cell (GMC) division, is a direct target of MUTE. Whether FLP involves in meristemoid differentiation is unknown. Through sensitized genetic screening of flp‐1, we identified a mute‐like (mutl) mutant with arrested meristemoids. The mutant carried a novel allele of the MUTE locus, i.e., mute‐4. Intriguingly, mute‐4 is a hypomorphic allele that exhibits wild‐type appearance with slightly delayed meristemoid‐to‐GMC transition, whereas it renders an unexpected mutl epidermis with most meristemoids arrested and very few stomata when combined with flp (flp mute‐4), suggesting that FLP is a positive regulator during this transition process. Consistently, the expression of FLP increased during GMC commitment, and the number of cells at this stage was markedly increased in flp. flp scrm double mutants produced arrested meristemoids similar to mute, and FLP was able to interact physically with SCRM. Taken together, our results demonstrate that FLP functions together with MUTE and SCRMs to direct meristemoid‐to‐GMC fate transition. Significance Statement The MUTE•SCREAM heterodimer is a master core complex coordinating meristemoid‐to‐guard mother cell (GMC) transition during stomatal development. However, whether additional transcription factors contribute to this process is difficult to determine, as the lack of MUTE function precludes meristemoid progression to GMC. We isolated the weak mutant mute‐4 and surprisingly found that FOUR LIPS, previously reported to limit GMC symmetric division, could form a heterodimer with SCREAMs to promote meristemoid‐to‐GMC fate transition.