NSCLC is the leading cause of cancer-related deaths worldwide, and its progression is often driven by dysregulated molecular mechanisms, many of which represent potential therapeutic targets.105-108 High expression of ACTL6A in NSCLC tissues and cells has been linked to worse clinical outcomes, with suppression of ACTL6A expression leading to significant inhibition of NSCLC cell growth and increased apoptosis.109,110 Mechanistically, ACTL6A overexpression downregulates WWC1, a known inhibitor of YAP activation, in NCI-H2170 cells, while ACTL6A-targeting shRNA increases WWC1 expression. This evidence concerns the gene WWC1 and cancer.