PTK2 and neoplasm: In line with our prior work demonstrating synergy between MEK and FAK dual inhibition in UVM [25], these observations highlight ERK reactivation as a recurrent and potent escape route for GNAQ-driven tumor cells, and also reveal that the constitutively active FAK-Y180I/M183A mutant can preserve cellular viability when MEK activity is pharmacologically suppressed (Figure 2A–C).