ITGB4 and neoplasm: Notably, Zheng et al. identified a rare population of CD24+ITGB4+Notchhi cells from a Kras-driven NSCLC mouse model, which drives tumor progression, and Notch3 has a specific and non-redundant function in mediating the propagation and self-renewal of tumor-propagating cells.137 Importantly, a co-expression analysis revealed that Notch1 exhibits opposite functional effects on angiogenesis and immune pathways in LUAD and LUSC, potentially contributing to the development of Notch1-dependent targeted therapy strategies for specific tumor subgroups within NSCLC.138