One of the most striking observations was that the greatest amplitude in expression of PJA1 and PJA2 occurred in glioblastomas [8], and correlated with a concomitant and significant decrease in expression levels of Smad3, which we have identified as a PJA1 substrate [6, 7], and as a key receptor that regulates TGF-β signaling molecules [9, 10]. The gene discussed is TGFB1; the disease is glioblastoma.