Mechanistically, they found that HSP90-enriched oral metastatic TDEs induce tumor-associated macrophage (TAM) polarization in M2 macrophages, supporting cancer progression, with simultaneous CDC37/HSP90α/β depletion attenuating the metastatic TDEs-driven tumor-initiating activity in oral cancer [27] (Figure 1A). Here, HSP90AB1 is linked to neoplasm.