As UCH-L1 deficiency inhibits Retinoic acid (RA)-induced differentiation of neuroblastoma tumor cells by regulating RA-induced AKT and ERK1/2 signaling activation [68], and considering the critical role of RA-stimulated ERK1/2 pathway activity in Stra8 expression and meiotic progression in fetal germ cells [69], one may speculate that UCH-l1 deficiency can lead to a similar outcome in Uch-l1−/− spermatogonia. Here, AKT1 is linked to neoplasm.