Although the function of H3.3G34R/V mutations are not fully understood, hESC models have shown that H3.3G34R along with knockout of ATRX and TP53 blocked differentiation and enhanced proliferation of tumor cells resembling interneuron progenitor cells in the ventral forebrain, but had no effect in ventral hindbrain spheroids (81). This evidence concerns the gene TP53 and neoplasm.