Additionally, receptor tyrosine kinases (RTKs), EGFR, HER2, and IL-6R/gp130-associated kinases like JAKs, which are involved in several growth factor signaling pathways, can also activate STAT3 and support tumor progression; hence, RTK inhibitors are actively being investigated alongside STAT3 inhibitors for their potential to block these resistance mechanisms and offer new treatment options for aggressive or neuroendocrine forms of prostate cancer [109,110]. The gene discussed is STAT3; the disease is neoplasm.