BOC (BOC cell adhesion associated, oncogene regulated) is a cell-surface receptor component that mediates cell-cell interactions and promotes myogenic differentiation. As a member of the immunoglobulin superfamily of cell adhesion molecules, BOC functions in nervous system development and axon guidance through positive regulation of myoblast differentiation and smoothened signaling pathways 1. BOC variants have emerged as causal factors in nonsyndromic orofacial clefts (NSOFCs). Exome sequencing identified four BOC variants (three missense: p.R407W, p.G436S, p.D1018N; one nonsense: p.R681X) in unrelated cleft palate cases and a multiplex family with microform cleft lip 2. These variants function as hypomorphic alleles, reducing BOC function. Notably, epistatic interactions occur wherein BOC loss-of-function variants antagonize gain-of-function GLI2 mutations within the Sonic hedgehog (SHH) pathway, demonstrating a two-locus inheritance model for NSOFC pathogenesis 2. In glioblastoma, BOC expression is regulated through post-transcriptional modification. NAT10-catalyzed N4-acetylcytidine (ac4C) modification of BOC mRNA enhances its stability and translational efficiency, promoting tumor progression 1. HIF1α-mediated transcriptional activation of NAT10 under hypoxic conditions further increases BOC mRNA modification, linking BOC to hypoxia-driven glioblastoma advancement 1. These findings establish BOC as a critical developmental gene and emerging oncogenic target.