AKT1 and neoplasm: Spatial correlation analysis reveals hmmyCAFs also drive T‐cell dysfunction via integrin signaling (α2β1/αvβ8 with tumor cells; α1β1 with T_NK cells) and activation of the POSTN‐αvβ3‐Akt/Wnt axis (Figure 6B,D), creating Wnt5a‐enriched niches that facilitate immune evasion.[42] Hypoxia‐mediated metabolic reprogramming (Figure 3G) and transcription factor‐driven differentiation (Figure 4G,H) epigenetically enforce their specialization.