In line with these observations, hypoxia-induced autophagy impaired cancer cell susceptibility to Natural killer (NK)-mediated killing and the activation of autophagy in hypoxic cells was involved in selective degradation of the pro-apoptotic NK-derived serine protease granzyme B. Inhibition of autophagy by targeting Beclin 1 restored granzyme B levels in hypoxic cells and induced tumor regression by facilitating NK-mediated tumor cell killing [95, 96]. Here, BECN1 is linked to neoplasm.