These lipophilic molecules are capable of: (i) disrupting cellular membranes, compromising integrity and inducing necro-apoptotic responses; (ii) inducing mitochondrial dysfunction, leading to cytochrome c release and intrinsic pathway activation [52]; (iii) triggering apoptotic signalling, as demonstrated by β-amyrin’s activation of p38/JNK and caspase-3/9 in various cancer models [46, 53, 54]. This evidence concerns the gene CASP3 and cancer.