AKT1 and cancer: These associations reinforce TROP-2’s role in cancer progression, consistent with mechanistic evidence from Li et al. and Guan et al., who showed that TROP-2 activates pro-oncogenic pathways—such as PI3K/AKT and ERK/JNK—thereby promoting cell proliferation, migration, and epithelial-mesenchymal transition (EMT), a hallmark of metastasis and therapeutic resistance [15, 17].