Indeed, the abrogation of p21, as well as that of IGFBP2, in senescent psoriatic keratinocytes resulted in an increase of apoptosis in both steady-state and cytokine treatment conditions, and it was caused, at least in part, by the intracellular activation of caspase 3 and of JNK protein, this last known to trigger pro-apoptotic mechanisms in human keratinocytes, and in particular, in the psoriasis context [44]. The gene discussed is CASP3; the disease is psoriasis.