Genetic alterations including mutation of TP53 and amplification of 1q23 leading to activation of the AMPK/PKA pathway, membrane molecules activating multiple signaling pathways such as NF-κB and PI3K-AKT, thus upregulating anti-apoptotic proteins and releasing a variety of inflammatory cytokines, and gene mutation and immune phenotype alteration promoting clonal evolution and dysregulation of cancer signaling pathways have all been demonstrated to lead to venetoclax resistance[30]. This evidence concerns the gene TP53 and cancer.