AVIL and neoplasm: Figure 2 summarizes the general interactions between AVIL and actin, demonstrating that AVIL can modulate many actin-based processes. The AVIL gene is overexpressed in nearly 100% of glioblastomas and was identified as a bona fide oncogene that is crucial for glioblastoma tumorigenesis [71]. In recent studies, we have shown that AVIL expression is abnormally upregulated in RMS, where silencing this gene results in a dramatic reduction in proliferation and migration, killing cancer cells and preventing tumor formation [61].