ITGA7 (integrin alpha-7) is a laminin receptor primarily expressed in skeletal muscle that functions as a key mediator of cell-matrix adhesion. 1 The protein exists as multiple isoforms generated through alternative splicing, with developmental and tissue-specific regulation. 1 2 ITGA7 maintains myofiber cytoarchitecture and structural integrity by linking the extracellular matrix to the internal actin cytoskeleton, functioning similarly to the dystrophin-glycoprotein complex. 3 During myogenic differentiation, ITGA7 facilitates myoblast localization at laminin-rich sites and is essential for muscle stem cell polarity and asymmetric cell division. 2 Alternative splicing of ITGA7 isoforms X1 and X2 is regulated by the RNA-binding protein QKI, with proper isoform balance critical for muscle regeneration. 2 Clinically, mutations in ITGA7 cause congenital muscular dystrophy due to integrin alpha-7 deficiency. 1 Gene delivery of human ITGA7 via adeno-associated virus significantly extended survival and reduced dystrophic features in severely affected mdx/utrn(-/-) mice, protecting against contraction-induced muscle damage. 3 Beyond muscle, ITGA7 acts as a tumor suppressor in colorectal cancer; its downregulation via promoter hypermethylation activates pro-metastatic PI3K/AKT/NF-κB signaling, while circular RNA circITGA7 inhibits cancer growth by suppressing Ras pathway activation. 4 5 These findings support ITGA7 as a potential therapeutic target for both muscular dystrophy and cancer.