Rather, a novel molecular mechanism underlying the role of NGF‐NGFR communication in the regulation of biological functions was revealed, according to which NGF‐NGFR communication inefficiency suppressed the organization of the mitotic spindle through HDAC1 unclear trans‐localization‐inhibited PREX1 expression, which ultimately promoted the quantitative exhaustion of T cells infiltrated in tumor tissues. This evidence concerns the gene HDAC1 and neoplasm.