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In this study, we examined the possible apoptotic mechanism of pepsin‐digested extract of Caulerpa microphysa (CME) in myelomonocytic leukemia (WEHI‐3) cells. Flow cytometry demonstrated that CME induced cell cycle arrest in the G0/G1 phase and stimulated reactive oxygen species (ROS) production and calcium release but caused a loss of the mitochondrial membrane potential (MMP). The results indicated that the protein levels of cyclin D, cyclin E, CDK6, CDK2 and Bcl‐2 decreased and those of p21, p27, p53, Bax, Bid, GRP78, GADD153, apoptosis‐inducing factor (AIF), caspase‐3 and caspase‐9 increased in WEHI‐3 cells after CME treatment. In conclusion, CME induced G0/G1 phase arrest, decreased MMP and increased Ca2+ release and ROS production in the WEHI‐3 cells. The results suggest that CME may have potential as an anticancer agent. Practical Applications Caulerpa microphysa (CME) has multiple functions and has been applied as natural seaweed extracts in the food and pharmaceutical industries. This study revealed for the first time that CME treatments inhibited the expression of the anti‐apoptotic protein and promoted the expression of pro‐apoptotic proteins. The results suggest that CME could be functional in food and pharmaceutical industries and could be an alternative anticancer medicine in the future.