Interestingly, p16Ink4a and SA-β-Gal expression can be driven by β-amyloid in senescent astrocytes; however, the accumulation of SA-β-gal depends on pRB (retinoblastoma) functionality and is associated with the p21WAF1-mediated senescence pathway, independently of SA-β-gal status [38,39]. The gene discussed is CDKN2A; the disease is retinoblastoma.