Although migrasomes generated from re‐expressing ITM2B1‐115 in ITM2B‐knockdown cells accelerated tumor growth and Ki67 expression, knocking down caspase‐7 in parallel cells abolished these functions of ITM2B1‐115 (Figure 5J,K), which not only confirmed the protumoral roles of active caspase‐7 but also suggested that ITM2B truncation facilitated tumor growth, probably by facilitating active caspase‐7 migracytosis. The gene discussed is ITM2B; the disease is neoplasm.