As all of the above-mentioned signaling molecules mediate effects related to cell proliferation, growth, viability, tumor initiation and tumor cell migration [26,27,28], effects likewise seen to be influenced following PTPRE silencing, we investigated ERK/p-ERK, SRC/pSRC, AKT/p-AKT, and SGK3/pSGK3 expression after PTPRE knockdown in order to reveal possible PTPRE downstream signaling mechanisms in etoposide-resistant RB cells. Here, PTPRE is linked to retinoblastoma.