TP53 and retinoblastoma: This is mainly due to the concomitant dysregulation of various signal transduction pathways like, Rb, p53, Wnt, Ras-ERK, etc. (Fig. 3) which may have an impact on the oncogenic properties of retinoblastoma through multiple mechanisms, including the acquisition of stem cell-like phenotype, EMT activation and metabolic rewiring [20–23].