Although the key mutation found in the GTPase RhoA in AITL patients (RHOAG17V) was not found in the plck-GAPDH mice, a similar mutation was found in this protein (RHOAT37M), with equivalent RhoaG17V function, namely, the inactivation of its binding to GTP, which favored the growth of tumor cells [18,25]. This evidence concerns the gene GAPDH and neoplasm.